The use of slice encoding for metal artifact correction (SEMAC) sequencing improves the diagnostic evaluation of graft integrity following anterior cruciate ligament reconstruction.

OBJECTIVES: To determine whether magnetic resonance imaging (MRI) with metal artifact reduction sequencing is superior to conventional knee MRI in the evaluation of an injured anterior cruciate ligament (ACL) graft, where visualisation on conventional MRI can be limited by the metal artifact from fixation devices. METHODS: Eighteen patients underwent conventional MRI sequence (proton density fat saturated [PDFS]) and two types of metal artifact reduction sequencing MRI (WARP, slice encoding for metal artifact correction (SEMAC); Siemens) following a secondary injury to their ACL reconstructed knee. Six raters with experience in knee MRI evaluation reviewed sagittal PDFS, WARP, and SEMAC sequences, providing semi-quantitative grades for visualisation and diagnostic confidence assessing the ACL, posterior cruciate ligament , menisci, tibial and femoral tunnel margins, and articular cartilage. Intra-class correlation coefficients for inter-rater reliability were evaluated. The 6-rater mean scores for the visualisation and diagnostic confidence derived from each sequence were compared using the Friedman test for multiple paired samples. RESULTS: No statistically significant difference in the ACL visualisation among the sequences was found (p â€‹= â€‹0.193). Further, a subgroup analysis was performed in cases evaluated as "moderately blurry" or "indistinct ACL visualisation" on PDFS (58% of cases). SEMAC significantly improved diagnostic confidence in ACL visualisation (p â€‹= â€‹0.041) and ACL graft rupture (p â€‹= â€‹0.044) compared to PDFS. There was no statistically significant difference in the inter-observer reliability between sequences. The WARP sequence added 2.84 â€‹± â€‹0.69 â€‹min, while SEMAC added 2.95 â€‹± â€‹0.40 â€‹min to the standard knee MRI scan time. CONCLUSION: use of the SEMAC metal reduction sequence significantly improved diagnostic accuracy and confidence in the detection of ACL graft rupture in cases where the ACL was moderately blurry or indistinct on the PDFS sequence. This sequence should be considered as an adjunct to conventional PDFS in cases where graft visualisation is limited by the metal artifact from fixation devices. LEVEL OF EVIDENCE: III.

Baseline characteristics of patients predicting suitability for rapid naltrexone induction.

BACKGROUND AND OBJECTIVES: Extended-release (XR) injection naltrexone has proved promising in the treatment of opioid dependence. Induction onto naltrexone is often accomplished with a procedure known as rapid naltrexone induction. The purpose of this study was to evaluate pre-treatment patient characteristics as predictors of successful completion of a rapid naltrexone induction procedure prior to XR naltrexone treatment. METHODS: A chart review of 150 consecutive research participants (N = 84 completers and N = 66 non-completers) undergoing a rapid naltrexone induction with the buprenorphone-clonidine procedure were compared on a number of baseline demographic, clinical and psychosocial factors. Logistic regression was used to identify client characteristics that may predict successful initiation of naltrexone after a rapid induction-detoxification. RESULTS: Patients who failed to successfully initiate naltrexone were younger (AOR: 1.040, CI: 1.006, 1.075), and using 10 or more bags of heroin (or equivalent) per day (AOR: 0.881, CI: 0.820, 0.946). Drug use other than opioids was also predictive of failure to initiate naltrexone in simple bivariate analyses, but was no longer significant when controlling for age and opioid use level. CONCLUSIONS: Younger age, and indicators of greater substance dependence severity (more current opioid use, other substance use) predict difficulty completing a rapid naltrexone induction procedure. Such patients might require a longer period of stabilization and/or more gradual detoxification prior to initiating naltrexone. SCIENTIFIC SIGNIFICANCE: Our study findings identify specific characteristics of patients who responded positively to rapid naltrexone induction.

Undetected Ultracet™ dependence in an adolescent with nonmalignant back pain.

Addiction to painkillers or other substances in pediatric and adolescent cases of noncancer chronic pain is an understudied phenomenon, even amidst documented increases in rates of prescription opioid use and misuse. Case studies can inform the training of clinicians in ethically negotiating a balance between optimizing analgesia and mitigating risk of aberrant drug-taking behaviors. This report discusses an 18-year-old woman with idiopathic scoliosis and clinical depression secondary to undertreated refractory chronic back pain who underwent surgery to correct pseudoarthrosis after a prior spinal instrumentation operation. This intervention in conjunction with a course of patient-controlled analgesia, hydromorphone, and outpatient tramadol, naproxen, methadone, and gabapentin was successful in addressing her long-standing lumbar pain. The patient, however, continued to complain to her pain management team of postsurgical discomfort and insisted on being prescribed Ultracet™ (acetaminophen-tramadol) rather than generic tramadol. The patient's eventual disclosure of severe withdrawal discomfort and history of covert abuse of Ultracet™ is discussed with respect to key warning signs, gaps, and contingencies in the screening, surgical, and pain management processes.

AAV2 mediated retrograde transduction of corticospinal motor neurons reveals initial and selective apical dendrite degeneration in ALS.

Corticospinal motor neurons (CSMN) are the cortical component of motor neuron circuitry, which controls voluntary movement and degenerates in diseases such as amyotrophic lateral sclerosis, primary lateral sclerosis and hereditary spastic paraplegia. By using dual labeling combined with molecular marker analysis, we identified AAV2-2 mediated retrograde transduction as an effective approach to selectively target CSMN without affecting other neuron populations both in wild-type and hSOD1(G93A) transgenic ALS mice. This approach reveals very precise details of cytoarchitectural defects within vulnerable neurons in vivo. We report that CSMN vulnerability is marked by selective degeneration of apical dendrites especially in layer II/III of the hSOD1(G93A) mouse motor cortex, where cortical input to CSMN function is vastly modulated. While our findings confirm the presence of astrogliosis and microglia activation, they do not lend support to their direct role for the initiation of CSMN vulnerability. This study enables development of targeted gene replacement strategies to CSMN in the cerebral cortex, and reveals CSMN cortical modulation defects as a potential cause of neuronal vulnerability in ALS.