Dynamic locking plate vs. simple cannulated screws for nondisplaced intracapsular hip fracture: A comparative study.

INTRODUCTION: Intracapsular hip fractures (ICHF) are a common cause of morbidity and mortality and pose a great economic burden on the health care systems. Appropriate surgical treatment requires balancing optimal outcomes with the cost of treatment to the health care system. While in elderly patients with displaced ICHF arthroplasty became the standard of care, the internal fixation method for conserving the femoral head in younger patients or in nondisplaced ICHF is still in debate. We compared a dynamic locking plate with the standard cancellous cannulated screws (CCS) for treatment of nondisplaced ICHF. METHODS: All patients treated with internal fixation for nondisplaced ICHF between July 2009 and December 2012 at our level one trauma center were included in this study. Patients treated with Targon FN (Aesculap) implants and CCS (Synthes) were compared. Charts were reviewed for demographics, intraoperative data and peri/post operative complications retrospectively. Radiographical analysis, pain (VAS), quality of life (SF12) and function (MHHS) data were prospectively gathered. RESULTS: One hundred and fifteen non-displaced ICHFs were treated with internal fixation, 81 with CCS and 34 with Targon FN implant; the mean follow-up was 19 and 28 months, respectively. Group fracture characteristics (Garden/Powel classification), and demographics, excluding age, were not significantly different. Post-operative revision rates of the Targon FN and CCS groups, perioperative complications were not statistically different (p>0.05). Quality of life (SF-12), function (Modified Harris Hip Score) and Visual Analogue Scale (VAS) pain scores were not statistical different. CONCLUSIONS: Complication rates and clinical outcomes for the treatment of nondisplaced ICHF with Targon FN and SCC showed no significant differences. Based on this evidence in consideration of the substantial cost differential between the Targon FN and SCC we suggest SCC for treatment of nondisplaced ICHF. LEVEL OF EVIDENCE: III.

PTSD as a criminal defense: a review of case law.

Posttraumatic stress disorder (PTSD) has been offered as a basis for criminal defenses, including insanity, unconsciousness, self-defense, diminished capacity, and sentencing mitigation. Examination of case law (e.g., appellate decisions) involving PTSD reveals that when offered as a criminal defense, PTSD has received mixed treatment in the judicial system. Courts have often recognized testimony about PTSD as scientifically reliable. In addition, PTSD has been recognized by appellate courts in U.S. jurisdictions as a valid basis for insanity, unconsciousness, and self-defense. However, the courts have not always found the presentation of PTSD testimony to be relevant, admissible, or compelling in such cases, particularly when expert testimony failed to show how PTSD met the standard for the given defense. In cases that did not meet the standard for one of the complete defenses, PTSD has been presented as a partial defense or mitigating circumstance, again with mixed success.

Hilar mossy cells share developmental influences with dentate granule neurons.

Mossy cells are the major class of excitatory neurons in the dentate hilus. Although mossy cells are involved in a range of physiological and pathological conditions, very little is known about their ontogeny. To gain insight into this issue, we first determined the developmental stage at which mossy cells can be reliably identified with the molecular markers calretinin and GluR2/3 and found that hilar mossy cells were first identifiable around the end of the 1st postnatal week. Birthdating studies combined with staining for these markers revealed that the appearance of mossy cells coincided with the first wave of dentate granule cell production during mid-gestation. Since mossy cells are born as the first granule cells are produced and it is believed that mossy cells originate from the neuroepithelium adjacent to the dentate progenitor zone, we examined to what extent the development of mossy cells is controlled by the same molecular pathways as that of granule cells. To do this, we analyzed the production of mossy cells in Lef1 and NeuroD mutant animals, in which granule cell production is disrupted during precursor proliferation or neuronal differentiation, respectively. The production of mossy cells was almost entirely lost in both mutants. Collectively, these data suggests that hilar mossy cells, unlike CA subfield pyramidal cells, are influenced by many of the same developmental cues as dentate granule cells.

Expression of SDF-1 and CXCR4 during reorganization of the postnatal dentate gyrus.

Previous studies have demonstrated that stromal cell-derived factor 1 (SDF-1) is crucial for early dentate development; however, the mouse mutants for this chemokine and its only receptor, CXCR4, are neonatally lethal, making conclusions about the role of these molecules in postnatal development difficult to sustain. Previous expression analyses have used single labeling, but the distribution of CXCR4 is complex and to determine the cell types expressing CXCR4 requires multiple marker labeling. In this study, we examined the distribution of SDF-1 and CXCR4 mRNAs during the first postnatal weeks, combining these markers with several other cell-type-specific markers. We found that SDF-1 has three sites of expression: (1) continuation of prenatal expression in the meninges; (2) expression in Cajal-Retzius cells occupying the molecular layer of the upper and lower blades of the dentate, and (3) the maturing dentate granule neurons themselves. The timing of expression in these three sites corresponds to alterations in the distribution of the primary cell types expressing CXCR4 during the same periods, notably the expression of CXCR4 in radial-glial-like GFAP-expressing dentate precursors and immature dentate granule neurons. Taken together, our data suggest potential ongoing roles for SDF-1/CXCR4 signaling in the dentate gyrus during the early postnatal period that will be tested in the future with more precise genetic approaches.

Stromal-derived factor-1 (CXCL12) regulates laminar position of Cajal-Retzius cells in normal and dysplastic brains.

Normal brain development requires a series of highly complex and interrelated steps. This process presents many opportunities for errors to occur, which could result in developmental defects in the brain, clinically referred to as malformations of cortical development. The marginal zone and Cajal-Retzius cells are key players in cortical development and are established early, yet there is little understanding of the factors resulting in the disruption of the marginal zone in many types of cortical malformation syndromes. We showed previously that treatment with methylazoxymethanol in rats causes marginal zone dysplasia with displacement of Cajal-Retzius cells to deeper cortical layers. Here we establish that loss of activity of the chemokine stromal-derived factor-1 (SDF1) (CXCL12), which is expressed by the leptomeninges, is necessary and sufficient to cause marginal zone disorganization in this widely used teratogenic animal model. We also found that mice with mutations in the main receptor for SDF1 (CXCR4) have Cajal-Retzius cells displaced to deeper cortical layers. Furthermore, by inhibiting SDF1 signaling in utero by intraventricular injection of a receptor antagonist, we establish that SDF1 signaling is required for the maintenance of Cajal-Retzius cell position in the marginal zone during normal cortical development. Our data imply that cortical layering is not a static process, but rather requires input from locally produced molecular cues for maintenance, and that complex syndromes of cortical malformation as a result of environmental insults may still be amenable to explanation by interruption of specific molecular signaling pathways.