We describe a Massachusetts Bureau of Substance Abuse Services’ (BSAS) initiative to disseminate the office-based opioid treatment with buprenorphine (OBOT-B) Massachusetts Model from its development at Boston Medical Center (BMC) to its implementation at fourteen community health centers (CHCs) beginning in 2007. The Massachusetts Collaborative Care Model for the delivery of opioid agonist therapy with buprenorphine, in which nurses working with physicians play a central role in the evaluation and monitoring of patients, holds promise for the effective expansion of treatment for opioid use disorders. The training of and technical assistance for the OBOT nurses as well as a limited program assessment are described. Data spanning 6 years (2007 – 2013) reports patient demographics, prior treatment for opioid use disorders, history of overdose, housing, and employment. The expansion of OBOT to the fourteen CHCs increased the number of physicians who were “waivered” (i.e., enabling their prescribing of buprenorphine) by 375%, from 24 to 114, within 3 years. During this period the annual admissions of OBOT patients to CHCs markedly increased. Dissemination of the Massachusetts Model of the Office-Based Opioid Treatment with Buprenorphine employing a collaborative care model with a central role for nursing enabled implementation of effective treatment for patients with an opioid use disorder at community health centers throughout Massachusetts while effectively engaging primary care physicians in this endeavor.

Mild traumatic brain injury (mTBI) is a significant national health concern and there is growing evidence that repetitive mTBI (rmTBI) can cause long-term change in brain structure and function. The mitochondrion has been suggested to be involved in the mechanism of TBI. There are noninvasive methods of determining mitochondrial dysfunction through biomarkers and spectroscopy. Mitochondrial dysfunction has been implicated in a variety of neurological consequences secondary to rmTBI through activation of caspases and calpains. The purpose of this review is to examine the mechanism of mitochondrial dysfunction in rmTBI and its downstream effects on neuronal cell death, axonal injury and blood–brain barrier compromise.

BackgroundRussia and Eastern Europe have one of the fastest growing HIV epidemics in the world. While countries in this region have implemented HIV testing within addiction treatment systems, linkage to HIV care from these settings is not yet standard practice. The Linking Infectious and Narcology Care (LINC) intervention utilized peer-led strengths-based case management to motivate HIV-infected patients in addiction treatment to obtain HIV care. This paper describes the protocol of a randomized controlled trial evaluating the effectiveness of the LINC intervention in St. Petersburg, Russia.Methods/designParticipants (n = 349) were recruited from the inpatient wards at the City Addiction Hospital in St. Petersburg, Russia. After completing a baseline assessment, participants were randomly assigned to receive either the LINC intervention or standard of care. Participants returned for research assessments 6 and 12 months post-baseline. Primary outcomes were assessed via chart review at HIV treatment locations.DiscussionLINC holds the potential to offer an effective approach to coordinating HIV care for people who inject drugs in Russia. The LINC intervention utilizes existing systems of care in Russia, minimizing adoption of substantial infrastructure for implementation.Trial Registration NCT01612455

This case report presents a patient presenting with pseudobulbar deficits, parkinsonism and dystonia from ODS, whose symptoms were resistant to levodopa but markedly responsive to pramipexole. Case Description A 42-year-old man with history of von Willebrand disease type 1 was prescribed desmopressin after a recent nasal septoplasty in the setting of epistaxis post-surgery. Within days of discharge, patient presented to the hospital with a seizure. His sodium at the time of presentation was 122 mEq/L which was corrected to 132 mEq/L within a period of 24 hours. After transfer to our institution, ODS was confirmed on MRI which showed T2 hyperintense lesion at the central pons as well as T1 hypointensities at the bilateral lentiform nuclei (Figures 1, 2). Hospital course was complicated by a seizure, locked-in syndrome for approximately 3 weeks, dysphagia, dysarthria and difficulty with bilateral hand coordination. He was eventually discharged to rehabilitation with some improvement of these symptoms but did not return to his baseline. Approximately 11 months after his first admission, he was re-admitted for worsening dysphagia, dysarthria and bilateral hand discoordination. The severity of the dysphagia progressed to the point where he required a PEG placement for sustenance. The patient could not speak and required a cellular device in order to communicate. In addition to inability to swallow, he could not use his hands to write, hold a