Stroke remains a significant unmet clinical need with few treatment options that have a very narrow therapeutic window, thereby causing massive mortality and morbidity in the United States and around the world. Accordingly, finding safe and effective novel treatments with a wider therapeutic window stands as an urgent need in stroke. The progressive inflammation that occurs centrally and peripherally after stroke serves as a unique therapeutic target to retard and even halt the secondary cell death. Stem cell therapy represents a potent approach that can diminish inflammation in both the stroke brain and periphery (eg, spleen), advancing a paradigm shift from a traditionally brain-focused therapy to treating stroke as a neurological disorder with a significant peripheral pathology. The purpose of this review article is to highlight the inflammation-mediated secondary cell death that plagues both brain and spleen in stroke and to evaluate the therapeutic potential of stem cell therapy in dampening these inflammatory responses.

Stem cell transplantation with rehabilitation therapy presents an effective stroke treatment. Here, we discuss current breakthroughs in stem cell research along with rehabilitation strategies that may have a synergistic outcome when combined together after stroke. Indeed, stem cell transplantation offers a promising new approach and may add to current rehabilitation therapies. By reviewing the pathophysiology of stroke and the mechanisms by which stem cells and rehabilitation attenuate this inflammatory process, we hypothesize that a combined therapy will provide better functional outcomes for patients. Using current preclinical data, we explore the prominent types of stem cells, the existing theories for stem cell repair, rehabilitation treatments inside the brain, rehabilitation modalities outside the brain, and evidence pertaining to the benefits of combined therapy. In this review article, we assess the advantages and disadvantages of using stem cell transplantation with rehabilitation to mitigate the devastating effects of stroke.

Stem cell therapy may present an effective treatment for metastatic brain cancer and glioblastoma. Here we posit the critical role of a leaky blood-brain barrier (BBB) as a key element for the development of brain metastases, specifically melanoma. By reviewing the immunological and inflammatory responses associated with BBB damage secondary to tumoral activity, we identify the involvement of this pathological process in the growth and formation of metastatic brain cancers. Likewise, we evaluate the hypothesis of regenerating impaired endothelial cells of the BBB and alleviating the damaged neurovascular unit to attenuate brain metastasis, using the endothelial progenitor cell (EPC) phenotype of bone marrow-derived mesenchymal stem cells. Specifically, there is a need to evaluate the efficacy for stem cell therapy to repair disruptions in the BBB and reduce inflammation in the brain, thereby causing attenuation of metastatic brain cancers. To establish the viability of stem cell therapy for the prevention and treatment of metastatic brain tumors, it is crucial to demonstrate BBB repair through augmentation of vasculogenesis and angiogenesis. BBB disruption is strongly linked to metastatic melanoma, worsens neuroinflammation during metastasis, and negatively influences the prognosis of metastatic brain cancer. Using stem cell therapy to interrupt inflammation secondary to this leaky BBB represents a paradigm-shifting approach for brain cancer treatment. In this review article, we critically assess the advantages and disadvantages of using stem cell therapy for brain metastases and glioblastoma.

Patients who are bedridden often suffer from muscular atrophy due to reduced daily activities and can become depressed. However, patients who undergo physical therapy sometimes demonstrate positive benefits including a reduction of stressful and depressed behavior. Regenerative medicine has seen improvements in two stem cell-based therapies for central nervous system disorders. One therapy is through the transfer of exogenous stem cells. The other therapy is a more natural method and focuses on the increasing endogenous neurogenesis and restoring the neurological impairments. This study overviews how immobilization-induced disuse atrophy affects neurogenesis in rats, specifically hypothesizing that immobilization diminishes circulating trophic factor levels, like vascular endothelial growth factors or brain-derived neurotrophic factor, which in turn limits neurogenesis. This hypothesis requires the classification of the stem cell microenvironment by probing growth factors in addition to other stress-related proteins that correlate with exercise-induced neurogenesis. There is research examining the effects of increased exercise on neurogenesis while limiting exercise, which better demonstrates the pathological states of immobile stroke patients, remains relatively unexplored. To examine the effects of immobilization on neurogenesis quantitative measurements of movements, 5-bromo-2deoxyuridine labeling of proliferative cells, biochemical assays of serum, cerebrospinal fluid and neurological levels of trophic factors, growth factors, and stress-related proteins will indicate levels of neurogenesis. In further research, studies are needed to show how in vivo stimulation, or lack thereof, affects stem cell microenvironments to advance treatment procedures for strengthening neurogenesis in bedridden patients. This paper is a review article. Referred literature in this paper has been listed in the references section. The datasets supporting the conclusions of this article are available online by searching various databases, including PubMed. Some original points in this article come from the laboratory practice in our research center and the authors’ experiences.

Herpes simplex encephalitis is a rare disease presentation that is usually characterized by its temporal involvement and positive cerebrospinal fluid (CSF) polymerase chain reaction (PCR) for the herpes simplex virus (HSV). HSV PCR has a sensitivity of 96% and specificity of 99%. Even when the test is negative, if clinical suspicion is high, acyclovir therapy should be continued with a repeated PCR within a week. In this case, we report a 75-year-old female patient who presented with signs of hypertensive emergency with rapid deterioration to seizure-like activity on electroencephalogram (EEG) and signs of temporal encephalitis on magnetic resonance imaging (MRI). The patient did not respond to the initial regimen of antibiotics but did show significant clinical response to acyclovir though she had a negative CSF PCR for HSV ten days after the start of her neurological symptoms. In this case, we argue that alternative methods of diagnosis should be considered in cases of acute encephalitis. Our patient had negative PCR but her computerized tomography (CT), EEG, and MRI results pointed to temporal encephalitis caused by HSV.

Post-Coronavirus disease 2019 (COVID-19) development of polymyositis is rare, with very few cases documented in the literature. In patients developing vague symptoms after recovery from COVID-19, it is important to investigate all avenues, including the possibility of polymyositis. Polymyositis is typically characterized as symmetrical muscle weakness and histological, electrical, and chemical evidence of muscle injury. Patients identified can be treated with immunosuppressants to return some quality of life and prevent disease progression. In this report, we describe a 58-year-old Caucasian male who presented with symptoms of weakness, myalgias, and arthralgias, six months after recovering from flu-like symptoms of COVID-19. The patient was tested for other autoimmune etiologies and myopathies without positive results. He was treated with prednisone and reported moderate improvement in symptoms. Unfortunately, the patient declined a muscle biopsy or electromyographic testing. According to the criteria for polymyositis set by the Myositis Association and the response to therapy, the patient's symptoms pointed to a likely diagnosis of post-COVID-19 polymyositis.

Follicular dendritic cells help advance B-Cells in becoming memory B-Cells or antibody-producing plasma cells in the light zone, or undergo additional affinity maturation in the dark zone. Follicular dendritic cell sarcoma (FDCS) is an extremely rare soft tissue malignancy derived from follicular dendritic cells. Autoimmune disease increases the risks for the development of hematological malignancies. To the best of our knowledge, there are few cases of FDCS development in the setting of underlying Sjogren's syndrome (SS). Therefore, in this report, we present a novel case of FDCS associated with new-onset SS. In SS, the follicular dendritic cells are organized within germinal centers within the glands it infiltrates and is involved in B-Cell development. Because FDCS is derived from follicular dendritic cells, our report postulates that the unregulated follicular dendritic cell proliferation that may occur in SS could increase the risk for FDCS. Due to this possible connection observed in our patient, we highlight FDCS as a differential diagnosis when considering soft tissue cancers. We urge additional research to outline and explore the possible pathologic link between SS and FDCS.

Coronavirus disease 2019 (COVID-19) represents a multisystem disease that has caused a devastating global pandemic. The COVID-19 vaccine produced in response to the pandemic has been effective but can have side effects. One well-established condition is the reactivation of herpes zoster (HZ). Various risk factors increase the risk of HZ reactivation such as age, infections, and immunosuppressed states. HZ can have severe complications, including herpes zoster ophthalmicus and postherpetic neuralgia. Here, we present a unique case where a patient experienced HZ reactivation after both primary doses of the COVID-19 vaccine despite receiving early antiviral treatment.