Discussions between patients with chronic pain and their primary care provider about opioids and pain relief during routine clinic encounters.

OBJECTIVE: Existing studies indicate low levels of trust and shared decision making exist in the process of prescribing opioids for noncancer pain. Patient-provider communication has not been compared between patients receiving non-opioid pain medication, and those receiving opioids. This pilot study evaluated communication about pain management between patients with noncancer pain and their provider. DESIGN: Patient encounters with a primary care provider (PCP) were audio-recorded, followed by a short patient questionnaire to measure physician trust, depression, and anxiety. SETTING: Data were collected (October 2016-May 2017) at a primary care clinic in Saint Louis, MO. PATIENTS: Patients with noncancer chronic pain, receiving a nonsteroidal anti-inflammatory drug (NSAID) or an opioid with and without an NSAID. METHODS: Medical conversation analysis guided data interpretation of codes and themes. RESULTS: Themes were framed around stages of the routine PCP encounter (ie, opening, presenting complaint, examination, diagnosis, treatment, and closing). Themes within these stages included: managing stability (opening stage), fixation with pain (presenting complaint), changing the subject (examination stage), difficult conversations (diagnosis stage), patients chose protest or acceptance (treatment), and taking what you can get (closing). CONCLUSIONS: Much of the treatment of chronic pain, as a result of opioid prescriptions, revolves around negotiations about whether to use opioids or not. Patient education is required to disseminate realistic expectations regarding pain relief and risks of long-term opioid use. This may reduce patients' focus on pain severity and difficult conversations and increase shared decision making.

Ahr and Cyp1a2 genotypes both affect susceptibility to motor deficits following gestational and lactational exposure to polychlorinated biphenyls.

Polychlorinated biphenyls (PCBs) are persistent organic pollutants known to cause adverse health effects and linked to neurological deficits in both human and animal studies. Children born to exposed mothers are at highest risk of learning and memory and motor deficits. We developed a mouse model that mimics human variation in the aryl hydrocarbon receptor and cytochrome P450 1A2 (CYP1A2) to determine if genetic variation increases susceptibility to developmental PCB exposure. In our previous studies, we found that high-affinity AhrbCyp1a2(-/-) and poor-affinity AhrdCyp1a2(-/-) knockout mice were most susceptible to learning and memory deficits following developmental PCB exposure compared with AhrbCyp1a2(+/+) wild type mice (C57BL/6J strain). Our follow-up studies focused on motor deficits, because human studies have identified PCBs as a potential risk factor for Parkinson's disease. Dams were treated with an environmentally relevant PCB mixture at gestational day 10 and postnatal day 5. We used a motor battery that included tests of nigrostriatal function as well as cerebellar function, because PCBs deplete thyroid hormone, which is essential to normal cerebellar development. There was a significant effect of PCB treatment in the rotarod test with impaired performance in all three genotypes, but decreased motor learning as well in the two Cyp1a2(-/-) knockout lines. Interestingly, we found a main effect of genotype with corn oil-treated control Cyp1a2(-/-) mice performing significantly worse than Cyp1a2(+/+) wild type mice. In contrast, we found that PCB-treated high-affinity Ahrb mice were most susceptible to disruption of nigrostriatal function with the greatest deficits in AhrbCyp1a2(-/-) mice. We conclude that differences in AHR affinity combined with the absence of CYP1A2 protein affect susceptibility to motor deficits following developmental PCB exposure.

Integrating mental health professionals in residencies to reduce health disparities.

Health disparities in primary care remain a continual challenge for both practitioners and patients alike. Integrating mental health services into routine patient care has been one approach to address such issues, including access to care, stigma of health-care providers, and facilitating underserved patients' needs. This article addresses examples of training programs that have included mental health learners and licensed providers into family medicine residency training clinics. Descriptions of these models at two Midwestern Family Medicine residency clinics in the United States are highlighted. Examples of cross-training both medical residents and mental health students are described, detailing specific areas where this integration improves mental health and medical outcomes in patients. Challenges to effective integration are discussed, including larger system buy-in, medical providers' knowledge of mental health treatment, and the skills for clinical providers to possess in order to present mental health options to patients. Patients who traditionally experience multiple barriers to mental health treatment now have increased access to comprehensive care. As a result of more primary care clinics ascribing to an integrated care model of practice, providers may benefit from not only increased coordination of patient services but also utilizing behavioral health professionals to address health barriers in patients' lives.

Comparison of Neurological Function in Males and Females from Two Substrains of C57BL/6 Mice.

The C57BL/6 (B6) mouse is the background strain most frequently used for genetically-modified mice. Previous studies have found significant behavioral and genetic differences between the B6J (The Jackson Laboratory) and B6N substrains (National Institutes of Health); however, most studies employed only male mice. We performed a comprehensive battery of motor function and learning and memory tests on male and female mice from both substrains. The B6N male mice had greater improvement in the rotarod test. In contrast, B6J female mice had longer latencies to falling from the rotarod. In the Morris water maze (MWM), B6J males had significantly shorter latencies to finding the hidden platform. However, B6N females had significantly shorter path lengths in the reversal and shifted-reduced phases. In open field locomotor activity, B6J males had higher activity levels, whereas B6N females took longer to habituate. In the fear conditioning test, B6N males had a significantly longer time freezing in the new context compared with B6J males, but no significant differences were found in contextual or cued tests. In summary, our findings demonstrate the importance of testing both males and females in neurobehavioral studies. Both factors (sex and substrain) must be taken into account when designing developmental neurotoxicology studies.

Ahrd Cyp1a2(-/-) mice show increased susceptibility to PCB-induced developmental neurotoxicity.

Polychlorinated biphenyls (PCBs) are developmental neurotoxicants that produce cognitive and behavioral changes in children exposed during gestation and lactation. Coplanar PCBs bind the aryl hydrocarbon receptor (AHR) and can be sequestered in liver by cytochrome P450 1A2 (CYP1A2). The AHR is a ligand-activated transcription factor which increases expression of the CYP1 family, including CYP1A2. Our previous work examining genetic susceptibility to developmental PCB neurotoxicity showed that Ahr(b)Cyp1a2(-/-) mice with the high-affinity Ahr(b) allele and lacking CYP1A2 were most susceptible while Ahr(b)Cyp1a2(+/+) and poor-affinity Ahr(d)Cyp1a2(+/+) mice were resistant. To follow up, a fourth line of mice was generated with the Ahr(d)Cyp1a2(-/-) genotype and compared with the background strain Ahr(b)Cyp1a2(+/+). Dams received a PCB mixture or the corn oil vehicle at gestational Day 10 (GD10) and postnatal Day 5 (PND5). Offspring were tested at PND60 in open field locomotor, acoustic startle with pre-pulse inhibition (PPI), novel object recognition and Morris water maze. Locomotor activity was increased in PCB-treated Ahr(b)Cyp1a2(+/+) mice, but no differences were seen in control vs. PCB-treated Ahr(d)Cyp1a2(-/-) mice. PCB-treated Ahr(d)Cyp1a2(-/-) mice had a higher baseline startle response and significantly reduced pre-pulse inhibition at the 74dB level compared with corn oil-treated controls (P<0.05). PCB-treated Ahr(d)Cyp1a2(-/-) mice had impairments in novel objective recognition (P<0.05) and during all three hidden platform phases of Morris water maze (P<0.01). Combined with our previous findings, these results indicate Cyp1a2 genotype is more important in susceptibility to PCB-induced deficits in learning and memory, but Ahr genotype appears more important when assessing acoustic startle-PPI and locomotor activity.