Opioid vs nonopioid prescribers: Variations in care for a standardized acute back pain case.

BACKGROUND: Opioid analgesics are effective and appropriate therapy for many types of acute pain. Epidemiologic evidence supports a direct relationship between increased opioid prescribing and increases in opioid use disorders and overdoses. OBJECTIVE: To tailor our residency curriculum, we designed and fielded an unannounced standardized patient (USP) case involving a patient with acute back pain who is requesting Vicodin (5/325 mg). We describe residents' case management and examine whether their management decisions, including opioid prescribing, were related to their core clinical skills. METHODS: Results are based on 50 (USP) visits with residents in 2 urban primary care clinics. Highly trained USPs portrayed a patient with acute lower back pain who was taking leftover Vicodin with effective pain relief but was running out. We describe how residents managed this case, using both USP report and chart review data, and compare summary clinical skills scores between those who prescribed Vicodin and those who did not. RESULTS: Of the 50 residents, 18 prescribed Vicodin (10-60 pills). Among those who did not prescribe (32/50), most (50%) prescribed ibuprofen. Eighty-three percent of the prescribers and 72% of nonprescribers ordered physical therapy (nonsignificant). Of the 18 prescribers, 13 documented checking the prescription monitoring database. Prescribers had significantly better communication scores than nonprescribers (relationship development: 80% vs. 58% well done, P = .029; patient education: 59% vs. 31% well done, P = .018). Assessment summary scores were also higher (60% vs. 46%) but not significantly (P = .060). Patient satisfaction and activation scores were higher in the prescribers than nonprescribers (71% vs. 39%, P = .004 and 48% vs. 26%, P = .034, respectively). CONCLUSIONS: Most Vicodin prescribers did not follow prescribing guidelines, and they demonstrated better communication and assessment skills than the nonprescribers. Results suggest the need to guide residents in using a systematic approach to prescribing opioids safely and to develop an acceptable alternative pain management plan when they decide against prescribing.

Cisplatin induced alterations in nociceptor developmental trajectory elicits a TrkA dependent platinum-based chemotherapy induced neuropathic pain.

Cisplatin-based chemotherapy is a common treatment for paediatric cancer. Unfortunately, cisplatin treatment causes neuropathic pain, a highly prevalent adverse health related complication in adult childhood cancer survivors. Due to minimal understanding of this condition, there are currently no condition tailored analgesics available. Here we investigated an alteration in nociceptor maturation that results in neuronal sensitisation and manifestation of cisplatin induced survivorship pain in a TrkA dependent manner. Cisplatin was administered (i.p. 0.1 mg/kg Postnatal day 14 and 16) to neonatal male and female Wistar rats and nociceptive behavioural assays were performed. In vitro studies utilised isolated neonatal dorsal root ganglia sensory neurons treated with cisplatin (5 µg/ml) to elucidate impact upon nociceptor activation and neurite growth, in combination with TrkA inhibition (GW441756 10 nM and 100 nM). Cisplatin treated male and female neonatal Wistar rats developed a delayed but lasting mechanical and heat hypersensitivity. Cisplatin administration led to increased TrkA expression in dorsal root ganglia sensory neurons. Nerve growth factor (NGF) induced TrkA activation led to sensory neuritogenesis and nociceptor sensitisation, which could be prevented through pharmacological TrkA inhibition (GW441756 either s.c. 100 nM or i.p. 2 mg/kg). Administration of TrkA antagonist suppressed cisplatin induced TRPV1 mediated nociceptor sensitisation and prevented cisplatin induced neuropathic pain. These studies provide greater understanding of the underlying mechanisms that cause cisplatin induced childhood cancer survivorship pain and allowing identification of potential therapeutic targets.

The Role of Vascular-Immune Interactions in Modulating Chemotherapy Induced Neuropathic Pain.

Chemotherapy causes sensory disturbances in cancer patients that results in neuropathies and pain. As cancer survivorships has dramatically increased over the past 10 years, pain management of these patients is becoming clinically more important. Current analgesic strategies are mainly ineffective and long-term use is associated with severe side effects. The issue being that common analgesic strategies are based on ubiquitous pain mediator pathways, so when applied to clinically diverse neuropathic pain and neurological conditions, are unsuccessful. This is principally due to the lack of understanding of the driving forces that lead to chemotherapy induced neuropathies. It is well documented that chemotherapy causes sensory neurodegeneration through axonal atrophy and intraepidermal fibre degeneration causing alterations in pain perception. Despite the neuropathological alterations associated with chemotherapy-induced neuropathic pain being extensively researched, underlying causes remain elusive. Resent evidence from patient and rodent studies have indicated a prominent inflammatory cell component in the peripheral sensory nervous system in effected areas post chemotherapeutic treatment. This is accompanied by modulation of auxiliary cells of the dorsal root ganglia sensory neurons such as activation of satellite glia and capillary dysfunction. The presence of a neuroinflammatory component was supported by transcriptomic analysis of dorsal root ganglia taken from mice treated with common chemotherapy agents. With key inflammatory mediators identified, having potent immunoregulatory effects that directly influences nociception. We aim to evaluate the current understanding of these immune-neuronal interactions across different cancer therapy drug classes. In the belief this may lead to better pain management approaches for cancer survivors.

Gold Digger or Video Girl: the salience of an emerging hip-hop sexual script.

Concerns have been expressed in the common discourse and scholarly literature about the negative influence of Hip-Hop on its young listeners' ideas about sex and sexuality. Most of the scholarly literature has focused on the impact of this urban, Black media on young African American girls' sexual self-concept and behaviours. In response to this discourse, Stephens and Phillips (2003) proposed a Hip-Hop sexual scripting model that theorises about specific sexual scripts for young African American women. Their model includes eight different sexual scripts including the Gold Digger script. The present study proposes a ninth emerging script - the Video Girl. Participants were 18 female African American college students, between the ages of 18 and 30 years old from a large urban public university in the Southwest USA. Using q-methodology the present study found support for the existence of a Video Girl script. In addition, the data indicates that this script is distinct but closely related to Stephens and Phillips' Gold Digger script. These findings support their theory by suggesting that Hip-Hop sexual scripts are salient and hold real meaning for this sample.