Revision Proximal Tibiofibular Joint Reconstruction for the Treatment of Chronic Instability Secondary to Suture Button Construct Failure.

Recurrent proximal tibiofibular joint (PTFJ) instability can result from nonanatomic repair using a suture button construct. During initial reconstruction, proper identification of anatomic landmarks is critical for proper placement of suture button construct components and successful patient outcomes. In cases of symptomatic recurrent instability, a PTFJ reconstruction revision is warranted to alleviate symptoms of pain and instability.

Proximal Tibial Opening Wedge Osteotomy for the Treatment of Posterior Knee Instability and Genu Recurvatum Secondary to Increased Anterior Tibial Slope.

Decreased posterior tibial slope has been associated with increased risk of graft failure and knee instability after posterior cruciate ligament (PCL) reconstruction. Premature physeal arrest at the tibial tubercle is a common cause of osseous genu recurvatum. Surgical management is recommended to correct the tibial slope and prolong the integrity of the PCL graft.

Tibial Tubercle Preserving Anterior Closing Wedge Proximal Tibial Osteotomy and ACL Tunnel Bone Grafting for Increased Posterior Tibial Slope in Failed ACL Reconstructions.

Anterior cruciate ligament reconstruction (ACLR) failure is multifactorial, but it is known that increased posterior tibial slope (PTS) leads to a greater likelihood of ACLR failure. This technical note describes the senior author's technique for performing an anterior closing wedge proximal tibial osteotomy, in which the osteotomy is made proximal to the tibial tubercle. This procedure is the first part of a staged surgery for patients with multiple failed ACLRs and increased sagittal plane PTS.

Medial Patellofemoral Ligament Reconstruction Using a Quadriceps Tendon Autograft in a Patient with Open Physes.

Recurrent patellar dislocations are correlated with an elevated risk for further patellar dislocations. Chronic patellar instability is a disabling issue for some patients and may require surgical intervention for proper treatment. Risk factors for recurrent dislocations include medial patellofemoral ligament (MPFL) tears, patella alta, trochlear dysplasia, and increased tibial tubercle to trochlear groove distance.

Multiple Ligament Reconstructions of the Knee and Posterolateral Corner.

Injuries to the knee involving multiple ligaments occur in a variety of circumstances and require careful assessment and planning. A wide constellation of injuries can occur with causes sufficiently traumatic to produce bicruciate ligament deficiency, and this technical report will describe diagnosis, treatment and rehabilitation for a knee dislocation with lateral injury (KD-III-L on the Schenk classification). Reconstruction in the acute setting is preferred, with anatomic-based, single-bundle anterior cruciate ligament reconstruction, double-bundle posterior cruciate ligament reconstruction, and anatomic reconstruction of the posterolateral corner using two grafts for the 3 primary posterolateral corner stabilizers.

Arthroscopic Excision of Bipartite Patella.

A bipartite patella usually presents as an incidental finding on radiographs because most cases are asymptomatic. However, some patients may present with pain and functional limitations. Conservative treatment is sufficient to resolve symptoms in most cases; however, a small minority of patients may require surgical management.

Medial Patellofemoral Reconstruction Using Quadriceps Tendon Autograft, Tibial Tubercle Osteotomy, and Sulcus-Deepening Trochleoplasty for Patellar Instability.

Recurrent patellar dislocations have been correlated with an elevated risk of further patellar dislocations, often requiring surgical treatment. Risk factors include medial patellofemoral ligament (MPFL) tears, patella alta, trochlear dysplasia, and an increased tibial tubercle-trochlear groove distance. Surgical management must be based on a patient's unique joint pathoanatomy and may require MPFL reconstruction with tibial tubercle osteotomy or trochleoplasty either alone or in combination.

The Oblique Meniscomeniscal Ligament: A Case Report of a Rare Obstruction to Meniscal Root Repair.

Case: The authors present a case of a 41-year-old woman who was treated for a chronic type 2 posterior horn tear of the medial meniscal root. During an arthroscopic repair, a broad, thick ligament coursing through the intercondylar notch caused difficulty in visualizing the posterior joint space and necessitated creation of an accessory portal. Given its course and attachments, this structure was an example of a rare variant of anatomy, an oblique meniscomeniscal ligament.

Arthroscopic-Assisted Lateral Meniscal Allograft Transplantation With Open Ligamentous Extra-Articular Tenodesis.

Lateral meniscus allograft transplantation is performed in predominantly young, active patients and is an option to stabilize the joint in lateral meniscus-deficient patients after anterior cruciate ligament reconstruction. The lateral meniscus functions as an important restraint to anterior tibial translation, and meniscal transplant in such a patient may improve survivability of the graft in addition to preserving the patient's articular cartilage in the long term. A ligamentous extra-articular tenodesis procedure may be performed simultaneously to augment rotational stability of the joint, particularly in a patient with underlying ligamentous hyperlaxity.

Patellar Tendon Revision Reconstruction With Hamstring Tendon Autografts.

Patellar tendon rupture is an infrequent cause of disability in patients younger than 40 years, with chronic injury and repeat procedures creating difficulty in facilitating healing. Use of hamstring autograft to reinforce the repair has been reported to strengthen the repair construct in patients with previous failure or chronic injury. This technique describes utilization of gracilis and semitendinosus tendon autografts to reconstruct the patellar tendon in a case of primary repair failure.

Neuropathic pain and SCI: Identification and treatment strategies in the 21st century.

Pain is a common complication in patients following spinal cord injury (SCI), with studies citing up to 80% of patients reporting some form of pain. Neuropathic pain (NP) makes up a substantial percentage of all pain symptoms in patients with SCI and is often complex. Given the high prevalence of NP in patients with SCI, proper identification and treatment is imperative.

Protocadherin 10 alters γ oscillations, amino acid levels, and their coupling; baclofen partially restores these oscillatory deficits.

Approximately one in 45 children have been diagnosed with Autism Spectrum Disorder (ASD), which is characterized by social/communication impairments. Recent studies have linked a subset of familial ASD to mutations in the Protocadherin 10 (Pcdh10) gene. Additionally, Pcdh10's expression pattern, as well as its known role within protein networks, implicates the gene in ASD.

Percutaneous or Open Reduction of Closed Tibial Shaft Fractures During Intramedullary Nailing Does Not Increase Wound Complications, Infection or Nonunion Rates.

Objective: To compare the incidence of complications (wound, infection, and nonunion) among those patients treated with closed, percutaneous, and open intramedullary nailing for closed tibial shaft fractures.

Design: Retrospective review.

Setting: Multiple trauma centers.

Sociability Deficits and Altered Amygdala Circuits in Mice Lacking Pcdh10, an Autism Associated Gene.

Background: Behavioral symptoms in individuals with autism spectrum disorder (ASD) have been attributed to abnormal neuronal connectivity, but the molecular bases of these behavioral and brain phenotypes are largely unknown. Human genetic studies have implicated PCDH10, a member of the δ2 subfamily of nonclustered protocadherin genes, in ASD. PCDH10 expression is enriched in the basolateral amygdala, a brain region implicated in the social deficits of ASD.

Lysosomal iron modulates NMDA receptor-mediated excitation via small GTPase, Dexras1.

Background: Activation of NMDA receptors can induce iron movement into neurons by the small GTPase Dexras1 via the divalent metal transporter 1 (DMT1). This pathway under pathological conditions such as NMDA excitotoxicity contributes to metal-catalyzed reactive oxygen species (ROS) generation and neuronal cell death, and yet its physiological role is not well understood.

Results: We found that genetic and pharmacological ablation of this neuronal iron pathway in the mice increased glutamatergic transmission.

Prospective MEG biomarkers in ASD: pre-clinical evidence and clinical promise of electrophysiological signatures.

Autism spectrum disorders (ASD) are characterized by social impairments and restricted/stereotyped behaviors and currently affect an estimated 1 in 68 children aged 8 years old. While there has been substantial recent focus on ASD in research, both the biological pathology and, perhaps consequently, a fully effective treatment have yet to be realized. What has remained throughout is the hypothesis that ASD has neurobiological underpinnings and the observation that both the phenotypic expression and likely the underlying etiology is highly heterogeneous.

Convergence of circuit dysfunction in ASD: a common bridge between diverse genetic and environmental risk factors and common clinical electrophysiology.

Most recent estimates indicate that 1 in 68 children are affected by an autism spectrum disorder (ASD). Though decades of research have uncovered much about these disorders, the pathological mechanism remains unknown. Hampering efforts is the seeming inability to integrate findings over the micro to macro scales of study, from changes in molecular, synaptic and cellular function to large-scale brain dysfunction impacting sensory, communicative, motor and cognitive activity.

Pyramidal cell selective ablation of N-methyl-D-aspartate receptor 1 causes increase in cellular and network excitability.

Background: Neuronal activity at gamma frequency is impaired in schizophrenia (SZ) and is considered critical for cognitive performance. Such impairments are thought to be due to reduced N-methyl-D-aspartate receptor (NMDAR)-mediated inhibition from parvalbumin interneurons, rather than a direct role of impaired NMDAR signaling on pyramidal neurons. However, recent studies suggest a direct role of pyramidal neurons in regulating gamma oscillations.

High fat diet produces brain insulin resistance, synaptodendritic abnormalities and altered behavior in mice.

Insulin resistance and other features of the metabolic syndrome are increasingly recognized for their effects on cognitive health. To ascertain mechanisms by which this occurs, we fed mice a very high fat diet (60% kcal by fat) for 17days or a moderate high fat diet (HFD, 45% kcal by fat) for 8weeks and examined changes in brain insulin signaling responses, hippocampal synaptodendritic protein expression, and spatial working memory. Compared to normal control diet mice, cerebral cortex tissues of HFD mice were insulin-resistant as evidenced by failed activation of Akt, S6 and GSK3β with ex-vivo insulin stimulation.

Parvalbumin cell ablation of NMDA-R1 causes increased resting network excitability with associated social and self-care deficits.

NMDA-receptor (NMDAR) hypofunction is strongly implicated in the pathophysiology of schizophrenia. Several convergent lines of evidence suggest that net excitation propagated by impaired NMDAR signaling on GABAergic interneurons may be of particular interest in mediating several aspects of schizophrenia. However, it is unclear which behavioral domains are governed by a net increase of excitation and whether modulating downstream GABAergic signaling can reverse neural and thus behavioral deficits.

Dysbindin-1 loss compromises NMDAR-dependent synaptic plasticity and contextual fear conditioning.

Genetic variants in DTNBP1 encoding the protein dysbindin-1 have often been associated with schizophrenia and with the cognitive deficits prominent in that disorder. Because impaired function of the hippocampus is thought to play a role in these memory deficits and because NMDAR-dependent synaptic plasticity in this region is a proposed biological substrate for some hippocampal-dependent memory functions in schizophrenia, we hypothesized that reduced dysbindin-1 expression would lead to impairments in NMDAR-dependent synaptic plasticity and in contextual fear conditioning. Acute slices from male mice carrying 0, 1, or 2 null mutant alleles of the Dtnbp1 gene were prepared, and field recordings from the CA1 striatum radiatum were obtained before and after tetanization of Schaffer collaterals of CA3 pyramidal cells.

Anterior thoracolumbar spine exposure: critical review and analysis.

Background: Indications for anterior thoracolumbar spine interbody fusion have expanded because of safe and expeditious surgical exposure that can be provided by the approach surgeon. In our practice, previous anterior interbody instrumentation, multiple disc level exposure, patient age, and body habitus are not surgical deterrents despite the potential for increased complications. The arterial and venous complications of anterior spine exposure have been well documented; however, the purpose of this study is to document the incidence of other complications, such as deep vein thrombosis (DVT), lymphedema, seroma/hematoma, wound infection, and hospital readmission and to determine whether outcome is influenced by the factors mentioned above.

MeCP2-mediated alterations of striatal features accompany psychomotor deficits in a mouse model of Rett syndrome.

Rett Syndrome (RTT) is a neurodevelopmental disorder caused by mutations in the methyl-CpG-binding protein 2 (MECP2) gene. Affected individuals develop motor deficits including stereotypic hand movements, impaired motor learning and difficulties with movement. To understand the neural mechanisms of motor deficits in RTT, we characterized the molecular and cellular phenotypes in the striatum, the major input nucleus of the basal ganglia that controls psychomotor function, in mice carrying a null allele of Mecp2.