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Transradial access (TRA) has gained traction in neurointerventions as studies continue to demonstrate improved access site safety and equivalent end artery effectiveness when compared with traditional transfemoral techniques. Herein, we describe the technical nuances of obtaining TRA with a focus on distal TRA, left TRA, and sheathless TRA using larger bore catheters. We also discuss various strategies to avoid access site conversion if radial artery spasm or radial anomalies are encountered and offer some solutions for forming the Simmons catheter especially when it cannot be performed in the descending aorta. Lastly, we provide some insights regarding contraindications to TRA.

Although studies have continued to demonstrate the advantages of transradial access (TRA) for neurointervention, radial artery spasm (RAS) has remained a frequent cause of TRA failure. Dotter and Judkins initially described a technique to dilate areas of peripheral vascular stenosis by advancing sequentially larger catheters across the lesion over a guidewire. We have presented our institutional experience with the use of a modified Dotter technique with long radial sheaths to dilate areas of proximal flow-limiting RAS. In the present study, we reviewed the use of the Dotter technique for alleviating RAS in patients undergoing TRA for neurointervention.We performed a retrospective review of all patients undergoing TRA for neurointervention at our institution from 2018 to 2020 to identify patients with proximal flow-limiting RAS. For the identified patients, a modified Dotter technique had been used to dilate the stenosis. The demographic and periprocedural data were assessed to identify any adverse outcomes.Four patients with severe proximal flow-limiting RAS were identified. In each case, a hydrophilic long radial sheath and vascular dilator were sequentially advanced through the stenosis. In all cases, repeat angiography demonstrated improvement of the spasm, and the final radial angiograms demonstrated persistent improvement in caliber and regularity of the vessel. Each procedure was also completed via TRA with no periprocedural complications.Our modified Dotter technique was effective in bypassing areas of severe proximal flow-limiting RAS, obviating the need for access site conversion. Additional studies are warranted to understand the implication of the angioplasty-like effects seen within the radial artery after removal of the long radial sheaths.

Studies evaluating robotic guidance in lumbar fusion are limited primarily to evaluation of screw accuracy and perioperative complications. This is the first study to evaluate granular differences in short and long-term complication and revision rate profiles between robotic (RG) fluoroscopic (FG) guidance for minimally invasive short-segment lumbar fusions. A retrospective analysis of a prospective, multi-center database was performed. Complications were subdivided into surgical (further subcategorized into adjacent segment disease, new-onset back pain, radiculopathy, motor-deficit, hardware failure, pseudoarthrosis), wound, and medical complications. Complication and revision rates were compared between RG and FG groups cumulatively at 30, 90 days, and 1 year. 374 RG and 111 FG procedures were performed. RG was associated with an 86.25, 83.20, and 69.42% cumulative reduction in complication rate at 30, 90 days, and 1 year, respectively, compared to FG (p 0.001). At all follow-up points, new-onset radiculopathy and medical complications were most prevalent in both groups. The greatest reductions in complication rates were seen for new-onset back pain (88.13%; p = 0.001) and wound complications (95.05%; p 0.001) at 30 days, new-onset motor deficits (90.11%; p = 0.004) and wound complications (85.16%; p 0.001) at 90 days, and new-onset motor deficits (85.16%; p = 0.002), wound (85.16%; p 0.001), and medical complications (75.72%; p 0.001) at 1 year. RG was associated with a 92.58% (p = 0.002) reduction in revision rate at 90 days and a 66.08% (p = 0.026) reduction at 1 year. RG was associated with significant reductions in postoperative complication rates at all follow-up time points and significant reductions in revision rates at 90 days and 1 year.

Objective The purpose of this study is to highlight the relationship between obstructive hydrocephalus, changes in intracranial pressure, and sensorineural hearing loss. Methods A case of a 10-month old infant with sensorineural hearing loss secondary to obstructive hydrocephalus is reported. A literature review, with a focus on sensorineural hearing loss in the setting of changes in intracranial pressure, was performed. Results The authors report the case of a 10-month old infant with metopic and bicoronal craniosynostosis who presented with bilateral moderately severe sensorineural hearing loss after failing newborn hearing screening. Imaging subsequently demonstrated obstructive hydrocephalus, which was treated with the insertion of a VP shunt. The patient had immediate improvement of her hearing post-operatively, with repeat hearing tests showed resolution of her hearing loss. Conclusion Sensorineural hearing loss is a rare complication of hydrocephalus, but changes in intracranial pressure should be considered in the differential diagnosis. We put forth a flow diagram illustrating the hypothesized relationship between intracranial pressures, alterations in the levels of cochlear fluid, and hearing.

Purpose of review Sensorineural hearing loss (SNHL) is the most common sensory birth defect. The purpose of this article is to review the advances in next-generation sequencing (NGS) and molecular diagnosis of hereditary hearing loss. Recent findings Early diagnosis and detection of SNHL is critical for the development of appropriate speech and language, as neuroplasticity peaks in the first few years of life. There has been increased accuracy of NGS genetic testing, which has helped created a paradigm shift in the diagnosis of hearing loss. The diagnostic yield of genetic testing now approaches that of radiographic imaging; however, there remains a difference in cost and time delay. With the introduction of comprehensive genetic panels, 23-129 genes can be sequenced from the same blood sample. Summary Diagnostic genetic testing of SNHL in the past has been confined to a few genes through Sanger sequencing. The advent of NGS allows for development of comprehensive genetic panels, which test for up to 129 genes while improving the accuracy and efficiency of testing. This type of testing may become more common as the costs decrease and more genes are discovered.

Transcranial masses in the infant population can leave considerable skull base defects following resection. Traditional reconstructive techniques can result in significant morbidity or poor cosmetic results. We present a case of a large skull base defect in a six week-old infant, after removal of a giant cranio-cervicofacial teratoma, which was reconstructed using a versatile submental island flap. Additionally, preoperative planning and intraoperative navigation was advanced with the use of a 3D constructed model of the patient's mass.

BACKGROUND: Presence of non-autologous major histocompatibility complex class I (MHC-I) molecules on the surface of the grafted cells is one of the main reasons for their rejection in non-syngeneic hosts. We present a straightforward strategy to decrease the presence of MHC-I by shRNA inhibition of beta-2-microglobulin (B2M), a conservative light chain of MHC-I, on the surface of two main cell types that are used to engineer heart tissue constructs. METHODS AND RESULTS: Engineered heart tissue constructs can be generated by combining mouse WT19 fibroblasts and mouse embryonic stem cell-derived cardiac myocytes (mESC-CM). WT19 fibroblasts were stably transduced with an anti-B2M shRNA, which yielded a cell line with dramatically reduced B2M expression levels (16±11% of mock treated control cell line). Interferon gamma treatment increased the levels of B2M expression by >3-fold in both control and transduced fibroblasts; yet, B2M expression levels still remained very low in the transduced cells. When compared with their unmodified counterparts, transduced fibroblasts caused 5.7-fold lesser activation of cognate T-cells. B2M depletion in mESC-CM was achieved by 72h transduction with anti-B2M shRNA lentiviral particles. Transduced mESC-CM exhibited regular beating and expressed classical cardiac markers. When compared with their unmodified counterparts, transduced mESC-CM caused 2.5-fold lesser activation of cognate T-cells. In vivo assessment of B2M downregulation was performed by analyzing the preferential survival of B2M-downregulated cells in the intraperitoneal cavity of allogeneic mice. Both B2M-downregulated fibroblasts and B2M-downregulated myocytes survived significantly better when compared to their unmodified counterparts (2.01±0.4 and 5.07±1.6 fold increase in survival, respectively). In contrast, when modified WT19 fibroblasts were injected into the intraperitoneal cavity of syngeneic C57Bl/6 mice, no significant survival advantage was observed. Notably, the preferential survival of B2M-downregulated cells persisted in allogeneic hosts with normal levels of natural killer cells, although the effect was lesser in magnitude. CONCLUSIONS: Use of shRNA against beta-2-microglobulin offers a simple and effective approach to minimize immunogenicity of the main cellular components of cardiac tissue constructs in non-syngeneic recipients.

This manuscript discusses the current surgical management of glioblastoma. This paper highlights the common pathophysiology attributes of glioblastoma, surgical options for diagnosis/treatment, current thoughts of extent of resection (EOR) of tumor, and post-operative (neo)adjuvant treatment. Glioblastoma is not a disease that can be cured with surgery alone, however safely performed maximal surgical resection is shown to significantly increase progression free and overall survival while maximizing quality of life. Upon invariable tumor recurrence, re-resection also is shown to impact survival in a select group of patients. As adjuvant therapy continues to improve survival, the role of surgical resection in the treatment of glioblastoma looks to be further defined.

A teenaged girlwas evaluated for loss of smell with a probable duration of years, but she was uncertain about exact duration. Her parents stated that at the age of 3 years she sustained minor trauma to her nose while at a playground but that she had not experienced any major head trauma. The patient had a history of frequent cough and congestion, seasonal allergies, monthly migraine headaches, and considerable nose congestion at night. She did not recall a history of recurrent sinusitis, snoring, or mouth breathing. Her family history was otherwise normal and did not include any pattern of familial anosmia or delayed puberty. She reported the ability to detect very strong odors but not subtle ones. She was even unable to smell smoke at times. Physical examination revealed a clinically significant hump on the dorsum of the nose consistent with minimal prior trauma, but no other abnormal findings. The patient failed the Penn smell tests, correctly identifying only 3 of the 11 smells. Flexible fiber-optic examination of the nose revealed no masses, polyps, or cysts. A magnetic resonance image of the anterior skull base demonstrated absent olfactory sulci (OS) and bilateral olfactory grooves containing minimal tissue (Figure, A, yellow arrowheads). The Figure, B, depicts normal OS (pink arrowheads) and bulbs (yellow arrowheads) from a different patient for comparison. Coronal T2-weighted magnetic resonance image A Comparison image from normal patient B

Our goal was to test a hypothesis that downregulation of MHC class I molecules via inhibition of beta2-microglobulin gene expression can minimize immunogenicity of non-cardiac fibroblasts and stem cell derived cardiomyocytes without impairing ability of these cells to form functional cardiac tissue. When co-cultured with mouse stem cell cardiomyocytes, two different types of non-cardiac mouse embryonic fibroblasts (NIH3T3 and WT19) supported the development of three-dimensional cardiac fibers. Fibroblasts had to be irradiated to ensure optimal growth, so that they did not overgrow non-replicating cardiomyocytes and a proper ratio of fibroblasts to cardiomyocytes was needed to create optimal fibers. The fibers also formed when both cell types underwent downregulation of MHC-I molecules. The latter was achieved by inhibition of beta2-microglobulin gene expression using shRNA technology and was confirmed by qPCR and FACS analyses. The downregulation of MHC-I molecules made fibroblasts and cardiomyocytes less susceptible to T-cell recognition in both in vitro and in vivo experiments. We conclude that readily obtainable non-cardiac fibroblasts can be used to engineer functional cardiac tissue and that downregulation of MHC-I can make such tissue less prone to immune rejection.

One of the major obstacles to repair damaged myocardium with embryonic stem cell derived cardiomyocytes (ESC-CM) is their rejection by non-syngeneic hosts. We aimed to reduce the immunogenicity of these cells by downregulation of MHC class I molecules (MHC-I) on their surface. Cardiomyocytes were derived from mouse ESC in which puromycin resistance gene is driven by a cardiac-specific promoter. They formed beating cardiomyocyte layers and expressed cardiac specific proteins. Interferon gamma treatment was used to mimic the effects of inflammatory stimuli on the expression of MHC-I. Transduction of ESC-CM with beta-2-microglobulin shRNA decreased expression of MHC-I in both interferon gamma-treated and untreated samples. When MHC-I downregulated ESC-CM were used as in vitro targets, activation of cognate T-lymphocytes was significantly reduced. Moreover, in vivo, MHC-I downregulated cells exhibited improved survival when injected i.p. into allogeneic, but not to syngeneic mice. To confirm that this strategy can be used for different cell types, the results were verified using W19 fibroblasts. In the past, ESC-CM have been shown to improve ischemic myocardium in syngeneic or immunocompromised animals. Inhibition of MHC-I via shRNA offers a simple approach to minimize the immunogenicity of these cells for use in allo- or xenogeneic recipients. Extension of this methodology to ESC of larger mammals can provide a source of less immunogenic cardiomyocytes for human heart repair.