Does Facial Fracture Management Require Opioids? A Pilot Trial of a Narcotic-Minimizing Analgesia Protocol for Operative Facial Trauma.

Opioid minimization in the acute postoperative phase is timely in the era of the opioid epidemic. The authors hypothesize that patients with facial trauma receiving multimodal, narcotic-minimizing pain management in the perioperative period will consume fewer morphine milligram equivalents (MMEs) while maintaining adequate pain control compared with a traditional analgesia protocol. An IRB-approved pilot study evaluating isolated facial trauma patients compared 10 consecutive prospective patients of a narcotic-minimizing pain protocol beginning in August 2020 with a retrospective, chart-reviewed cohort of 10 consecutive patients before protocol implementation. The protocol was comprised of multimodal nonopioid pharmacotherapy given preoperatively (acetaminophen, celecoxib, and pregabalin). Postoperatively, patients received intravenous (IV) ketorolac, scheduled acetaminophen, ibuprofen, and gabapentin. Oxycodone was reserved for severe uncontrolled pain. The control group had no standardized protocol, though opioids were ad libitum. Consumed MMEs and verbal Numeric Rating Scale (vNRS) pain scores (0-10) were prospectively tracked and compared with retrospective data. Descriptive and inferential statistics were run. At all recorded postoperative intervals, narcotic-minimizing subjects consumed significantly fewer MMEs than controls [0-8 h, 21.5 versus 63.5 ( P = 0.002); 8-16 h, 4.9 versus 20.6 ( P = 0.02); 16-24 h, 3.3 versus 13.9 ( P = 0.03); total 29.5 versus 98.0 ( P = 0.003)]. At all recorded postoperative intervals, narcotic-minimizing subjects reported less pain (vNRS) than controls (0-8 h, 7.7 versus 8.1; 8-16 h, 4.4 versus 8.0; 16-24 h 4.3 versus 6.9); significance was achieved at the 8 to 16-hour time point ( P = 0.006). A multimodal, opioid-sparing analgesia protocol significantly reduces opioid use in perioperative facial trauma management without sacrificing satisfactory pain control for patients.

Jugular Tubercle Meningioma with Hemorrhagic Conversion Mimicking a Ruptured Thrombosed Giant Vertebrobasilar Aneurysm.

BACKGROUND: Hemorrhagic meningiomas, although relatively uncommon, represent a distinct clinical entity. In some cases, these meningiomas can closely mimic a thrombosed aneurysm. We present a case of a jugular tubercle meningioma whose radiographic and clinical picture initially suggested a ruptured, thrombosed vertebrobasilar aneurysm. This case serves to highlight several key differences between these 2 pathologies that can assist in diagnosis. CASE DESCRIPTION: A 54-year-old woman presented to an outside hospital with a severe, sudden onset headache along with new-onset horizontal diplopia. On examination, she was noted to have a left sixth nerve palsy. A computerized tomography scan was performed and demonstrated a mass in the region of the left jugular foramen. A subsequent lumbar puncture was suggestive of subarachnoid hemorrhage. Frozen section was suggestive of meningioma and our patient underwent a successful gross total resection with no permanent neurological sequelae. CONCLUSIONS: Hemorrhagic meningiomas can have a clinical and radiologic picture that closely resembles a ruptured, thrombosed cerebral aneurysm. Based on our single case, we suggest several important diagnostic differentiators between these 2 entities. We found the hemorrhagic meningioma to exhibit eggshell-like rim calcification, thick, irregular peripheral enhancement, and a central cystic component. This can be contrasted to the classic appearance of a thrombosed aneurysm with mixed T1-, T2-weighted signal intensity, and occasional regular, thin peripheral enhancement.

Cell- and region-specific expression of depression-related protein p11 (S100a10) in the brain.

P11 (S100a10), a member of the S100 family of proteins, has widespread distribution in the vertebrate body, including in the brain, where it has a key role in membrane trafficking, vesicle secretion, and endocytosis. Recently, our laboratory has shown that a constitutive knockout of p11 (p11-KO) in mice results in a depressive-like phenotype. Furthermore, p11 has been implicated in major depressive disorder (MDD) and in the actions of antidepressants. Since depression affects multiple brain regions, and the role of p11 has only been determined in a few of these areas, a detailed analysis of p11 expression in the brain is warranted. Here we demonstrate that, although widespread in the brain, p11 expression is restricted to distinct regions, and specific neuronal and nonneuronal cell types. Furthermore, we provide comprehensive mapping of p11 expression using in situ hybridization, immunocytochemistry, and whole-tissue volume imaging. Overall, expression spans multiple brain regions, structures, and cell types, suggesting a complex role of p11 in depression. J. Comp. Neurol. 525:955-975, 2017. © 2016 Wiley Periodicals, Inc.

The influences of reproductive status and acute stress on the levels of phosphorylated delta opioid receptor immunoreactivity in rat hippocampus.

In the hippocampus, ovarian hormones and sex can alter the trafficking of delta opioid receptors (DORs) and the proportion of DORs that colocalize with the stress hormone, corticotropin releasing factor. Here, we assessed the effects of acute immobilization stress (AIS) and sex on the phosphorylation of DORs in the rat hippocampus. We first localized an antibody to phosphorylated DOR (pDOR) at the SER363 carboxy-terminal residue, and demonstrated its response to an opioid agonist. By light microscopy, pDOR-immunoreactivity (ir) was located predominantly in CA2/CA3a pyramidal cell apical dendrites and in interneurons in CA1-3 stratum oriens and the dentate hilus. By electron microscopy, pDOR-ir primarily was located in somata and dendrites, associated with endomembranes, or in dendritic spines. pDOR-ir was less frequently found in mossy fibers terminals. Quantitative light microscopy revealed a significant increase in pDOR-ir in the CA2/CA3a region of male rats 1h following an injection of the opioid agonist morphine (20mg/kg, I.P). To look at the effects of stress on pDOR, we compared pDOR-ir in males and cycling females after AIS. The level of pDOR-ir in stratum radiatum of CA2/CA3a was increased in control estrus (elevated estrogen and progesterone) females compared to proestrus and diestrus females and males. However, immediately following 30min of AIS, no significant differences in pDOR levels were seen across estrous cycle phase or sex. These findings suggest that hippocampal levels of phosphorylated DORs vary with estrous cycle phase and that acute stress may dampen the differential effects of hormones on DOR activation in females.

Ovarian hormones influence corticotropin releasing factor receptor colocalization with delta opioid receptors in CA1 pyramidal cell dendrites.

Stress interacts with addictive processes to increase drug use, drug seeking, and relapse. The hippocampal formation (HF) is an important site at which stress circuits and endogenous opioid systems intersect and likely plays a critical role in the interaction between stress and drug addiction. Our prior studies demonstrate that the stress-related neuropeptide corticotropin-releasing factor (CRF) and the delta-opioid receptor (DOR) colocalize in interneuron populations in the hilus of the dentate gyrus and stratum oriens of CA1 and CA3. While independent ultrastructural studies of DORs and CRF receptors suggest that each receptor is found in CA1 pyramidal cell dendrites and dendritic spines, whether DORs and CRF receptors colocalize in CA1 neuronal profiles has not been investigated. Here, hippocampal sections of adult male and proestrus female Sprague-Dawley rats were processed for dual label pre-embedding immunoelectron microscopy using well-characterized antisera directed against the DOR for immunoperoxidase and against the CRF receptor for immunogold. DOR-immunoreactivity (-ir) was found presynaptically in axons and axon terminals as well as postsynaptically in somata, dendrites and dendritic spines in stratum radiatum of CA1. In contrast, CRF receptor-ir was predominantly found postsynaptically in CA1 somata, dendrites, and dendritic spines. CRF receptor-ir frequently was observed in DOR-labeled dendritic profiles and primarily was found in the cytoplasm rather than at or near the plasma membrane. Quantitative analysis of CRF receptor-ir colocalization with DOR-ir in pyramidal cell dendrites revealed that proestrus females and males show comparable levels of CRF receptor-ir per dendrite and similar cytoplasmic density of CRF receptor-ir. In contrast, proestrus females display an increased number of dual-labeled dendritic profiles and an increased membrane density of CRF receptor-ir in comparison to males. We further examined the functional consequences of CRF receptor-ir colocalization with DOR-ir in the same neuron using the hormone responsive neuronal cell line NG108-15, which endogenously expresses DORs, and assayed intracellular cAMP production in response to CRF receptor and DOR agonists. Results demonstrated that short-term application of DOR agonist SNC80 inhibited CRF-induced cAMP accumulation in NG108-15 cells transfected with the CRF receptor. These studies provide new insights on opioid-stress system interaction in the hippocampus of both males and females and establish potential mechanisms through which DOR activation may influence CRF receptor activity.