Whole-brain volumetric microscopy techniques such as serial two-photon tomography (STPT) can provide detailed information on the roles of neuroinflammation and neuroplasticity throughout the whole brain post-stroke. STPT automatically generates high-resolution images of coronal sections of the entire mouse brain that can be readily visualized in three dimensions. We developed a pipeline for whole brain image analysis that includes supervised machine learning (pixel-wise random forest models via the “ilastik” software package) followed by registration to a standardized 3-D atlas of the adult mouse brain (Common Coordinate Framework v3.0; Allen Institute for Brain Science). These procedures allow the detection of cellular fluorescent signals throughout the brain in an unbiased manner. To illustrate our imaging techniques and automated image quantification, we examined long-term post-stroke motor circuit connectivity in mice that received a motor cortex photothrombotic stroke. Two weeks post-stroke, mice received intramuscular injections of pseudorabies virus (PRV-152), a trans-synaptic retrograde herpes virus driving expression of green fluorescent protein (GFP), into the affected contralesional forelimb to label neurons in descending tracts to the forelimb musculature. Mice were sacrificed 3 weeks post-stroke. We also quantified sub-acute neuroinflammation in the post-stroke brain in a separate cohort of mice following a 60 min transient middle cerebral artery occlusion (tMCAo). Naive e450+-labeled splenic CD8+ cytotoxic T cells were intravenously injected at 7, 24, 48, and 72 h post-tMCAo. Mice were sacrificed 4 days after stroke. Detailed quantification of post-stroke neural connectivity and neuroinflammation indicates a role for remote brain regions in stroke pathology and recovery. The workflow described herein, incorporating STPT and automated quantification of fluorescently labeled features of interest, provides a framework by which one can objectively evaluate labeled neuronal or lymphocyte populations in healthy and injured brains. The results provide region-specific quantification of neural connectivity and neuroinflammation, which could be a critical tool for investigating mechanisms of not only stroke recovery, but also a wide variety of brain injuries or diseases.

Deep Brain Stimulation (DBS) has revolutionized the lives of patients of Parkinson disease, offering therapeutic options to those not benefiting entirely from medications alone. With its proven track record of outperforming the best medical management, the goal is to unlock the full potential of this therapy. Currently, the Globus Pallidus Interna (GPi) and Subthalamic Nucleus (STN) are both viable targets for DBS, and the choice of site should focus on the constellation of symptoms, both motor and nonmotor, which are key determinants to quality of life. Our article sheds light on the specific advantages and drawbacks of the two sites, highlighting the need for matching the inherent properties of a target with specific desired effects in patients. UT Southwestern Medical Center has a robust and constantly evolving DBS program and the narrative from our center provides invaluable insight into the practical realities of DBS. The ultimate decision in selecting a DBS target is complex, ideally made by a multidisciplinary team, tailored towards each patient's profile and their expectations, by drawing upon scientific evidence coupled with experience. Ongoing research is expanding our knowledge base, which should be dynamically incorporated into an institute's DBS paradigm to ensure that patients receive the optimal therapy.

A 7-year-old female child was presented to the emergency room with acute abdominal pain and vaginal bleeding. Her assessment revealed a firm large lower abdominal mass with evidence of precocious puberty with bilaterally symmetrically enlarged breast (Tanner stage B4-P1-A1). Abdominal imaging showed a well-defined soft midline pelvi-abdominal single mass measuring 7.0×12.6×11.7 cms with no ascites. Serum tumour markers including lactate dehydrogenase (LDH), beta-subunit of human chorionic gonadotropin (B-hCG) and luteinizing hormone/follicular stimulating hormone (LH/FSH) were all normal. At operation, there was a huge abdominal tumour weighing 558 grams, localized to the right ovary sparing the left ovary, uterus, lymph nodes and other abdominal organs. Unilateral right salpingo-oophorectomy was performed. Histopathologic examination revealed ovarian dysgerminoma with intact capsule; FIGO Ia. Immunohistochemical stainings were positive for placental alkaline phosphatase (PALP), CD 117(c-kit) and calretinin focally but was negative for cancer antigen-125 (CA-125), B-hCG, S-100, carcinoembryonic antigen (CEA), and leukocyte common antigen (LCA). Being fitting in the low risk classification, the wait and see protocol was selected with strict follow-up with pediatric oncologist and pediatric surgeon. Along the duration of 2 years follow up, there was no more vaginal bleeding with dramatic reduction of the breast size and no recurrence.

Meniere's disease, with its characteristic symptom triad of vertigo, balance and hearing disorders has yet to have its pathophysiology outlined conclusively. Any theory must elucidate all aspects of the natural progression, including vestibular and auditory symptoms. While the central dogma revolves around endolymphatic hydrops, this theory is not without laws, such as its inability to explain all the physiological changes seen in patients, or the often absence of symptoms. While several degenerative changes are observed in temporal bone histopathology, they do not necessarily explain the sequence of events in the development and progress of the disease. This chapter explores the pathophysiology of the disease, focusing on the hydrops theory, while presenting evidence for and against it. Various changes in the inner ear physiology such as pressure changes, ionic disequilibrium, endocochlear potentials; in human and animal models are described. Alternative explanations for symptoms are discussed. This chapter touches briely upon etiology associated with Meniere's (and hydrops), and aims to assist a deeper understanding of the relationship of the process to clinical and experimental indings. A clear understanding of the process guides not only the clinical management to improve quality of life but also the direction of future research endeavors.

Hemorrhagic stroke accounts for 15% of all strokes but results in nearly a third of the mortality. Neuroimaging forms the mainstay in diagnosis, which has resulted in improved treatment outcomes. The mandate of neuroimaging includes management, risk assessment, prognostication, and research. This involves rapid identiication not only to direct treatment but also to discover the underlying etiology such as vascular malformations or tumors, monitor the evolving course of the hemorrhage and rapidly identify complications. While computed tomography (CT) remains the imaging of choice to rapidly detect acute hemorrhage, growing evidence shows that magnetic resonance imaging (MRI) is comparable to CT for detecting blood in the immediate seting and superior in this regard at subacute and chronic time points. Several advances have been made in the image sequencing protocols to detect bleeds at varying time points and to distinguish possible etiology. Initial and serial imaging is used to identify patients who may beneit from intervention. Advances in this ield such as difusion tensor imaging and functional MRI are being studied for their impact in understanding the extent of injury and possible recovery mechanisms, possibly allowing prognostication for patients.