scholarly journals Clinical Management of Moyamoya Patients

2021 ◽  
Vol 10 (16) ◽  
pp. 3628
Author(s):  
Isabella Canavero ◽  
Ignazio Gaspare Vetrano ◽  
Marialuisa Zedde ◽  
Rosario Pascarella ◽  
Laura Gatti ◽  
...  
Keyword(s):  
Randomized Clinical Trials ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Long Term Outcomes ◽  
Hemorrhagic Risk ◽  
Collateral Vessels ◽  
Hereditary Conditions ◽  
The Brain ◽  
Internal Carotid Arteries

Moyamoya angiopathy (MMA) is a peculiar cerebrovascular condition characterized by progressive steno-occlusion of the terminal part of the internal carotid arteries (ICAs) and their proximal branches, associated with the development of a network of fragile collateral vessels at the base of the brain. The diagnosis is essentially made by radiological angiographic techniques. MMA is often idiopathic (moyamoya disease-MMD); conversely, it can be associated with acquired or hereditary conditions (moyamoya Syndrome-MMS); however, the pathophysiology underlying either MMD or MMS has not been fully elucidated to date, and this poor knowledge reflects uncertainties and heterogeneity in patient management. MMD and MMS also have similar clinical expressions, including, above all, ischemic and hemorrhagic strokes, then headaches, seizures, cognitive impairment, and movement disorders. The available treatment strategies are currently shared between idiopathic MMD and MMS, including pharmacological and surgical stroke prevention treatments and symptomatic drugs. No pharmacological treatment able to reverse the progressive disappearance of the ICAs has been found to date in both idiopathic and syndromic cases. Antithrombotic agents are usually prescribed in ischemic MMA, although the coexisting hemorrhagic risk should be considered. Surgical revascularization techniques, which are currently the best available treatment in symptomatic MMA, are associated with good long-term outcomes and reduced ischemic and hemorrhagic risks. Given the lack of dedicated randomized clinical trials, current treatment is mainly based on observational studies and physicians’ and surgeons’ expertise.

scholarly journals Molecular mechanisms of cell death in neurological diseases

2021 ◽  
Author(s):  
Diane Moujalled ◽  
Andreas Strasser ◽  
Jeffrey R. Liddell
Keyword(s):  
Cell Death ◽  
Neurodegenerative Diseases ◽  
Molecular Mechanisms ◽  
Neuronal Development ◽  
Neurological Diseases ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Response To Therapy ◽  
Signalling Cascades ◽  
The Brain

AbstractTightly orchestrated programmed cell death (PCD) signalling events occur during normal neuronal development in a spatially and temporally restricted manner to establish the neural architecture and shaping the CNS. Abnormalities in PCD signalling cascades, such as apoptosis, necroptosis, pyroptosis, ferroptosis, and cell death associated with autophagy as well as in unprogrammed necrosis can be observed in the pathogenesis of various neurological diseases. These cell deaths can be activated in response to various forms of cellular stress (exerted by intracellular or extracellular stimuli) and inflammatory processes. Aberrant activation of PCD pathways is a common feature in neurodegenerative diseases, such as amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease, resulting in unwanted loss of neuronal cells and function. Conversely, inactivation of PCD is thought to contribute to the development of brain cancers and to impact their response to therapy. For many neurodegenerative diseases and brain cancers current treatment strategies have only modest effect, engendering the need for investigations into the origins of these diseases. With many diseases of the brain displaying aberrations in PCD pathways, it appears that agents that can either inhibit or induce PCD may be critical components of future therapeutic strategies. The development of such therapies will have to be guided by preclinical studies in animal models that faithfully mimic the human disease. In this review, we briefly describe PCD and unprogrammed cell death processes and the roles they play in contributing to neurodegenerative diseases or tumorigenesis in the brain. We also discuss the interplay between distinct cell death signalling cascades and disease pathogenesis and describe pharmacological agents targeting key players in the cell death signalling pathways that have progressed through to clinical trials.

Treatment strategies and long-term outcomes for primary intramedullary spinal germinomas: an institutional experience

2014 ◽  
Vol 121 (3) ◽  
pp. 541-548 ◽  
Author(s):  
Liang Wu ◽  
Tao Yang ◽  
Xiaofeng Deng ◽  
Chenlong Yang ◽  
Jingyi Fang ◽  
...  
Keyword(s):  
Treatment Strategies ◽  
Long Term Outcomes ◽  
Institutional Experience

Visualization of immature brain lesions: MR patterns of long-term outcomes. Case reports

2021 ◽  
Vol 2 (2) ◽  
pp. 94-99
Author(s):  
Anatoly V. Anikin ◽  
Milana A. Basargina ◽  
Eugeniya V. Uvakina
Keyword(s):  
White Matter ◽  
Premature Infants ◽  
Periventricular Leukomalacia ◽  
Brain Magnetic Resonance Imaging ◽  
Brain Lesions ◽  
Gestation Period ◽  
Long Term Outcomes ◽  
Immature Brain ◽  
The Brain

The periventricular and deep white matter of the immature brain of premature infants has an increased vulnerability to various, primarily ischemic injuries. The leading mechanism of selective vulnerability of the white matter of the large hemispheres in children with a low gestation period is the lack of formation of adjacent blood circulation zones between the main arteries of the developing brain. Magnetic resonance imaging has a high sensitivity to detect damage to the brain substance, both in the acute period and in the period of long-term outcomes. Periventricular leukomalacia (PVL) is one of the variants of brain damage in premature infants and the most common term in the conclusions of diagnostic doctors (ultrasound, CT, MRI). Considering the pathomorphological criteria, not always detected changes in the white matter of the large hemispheres are PVL. Diffuse (telencephalic) gliosis and diffuse leukomalacia are ordinary and typical variants of damage to the white matter of the large hemispheres in extremely premature infants, with a gestation period of up to 30-32 weeks. In the first variant, atrophic changes predominate with a pronounced decrease in the volume of white matter and a secondary expansion of the lateral ventricles. Diffuse leukomalacia is most often mistaken for PVL, but the localization of the white matter lesion of the large hemispheres is extensive and extends beyond the peri- and paraventricular region. Clinical examples show various variants of primary non-hemorrhagic brain lesions in prematurely born children in the long-term period. The analysis of the revealed changes is carried out, taking into account current data on developing the brain and pathomorphological criteria.

scholarly journals Short- and long-term outcomes of treatment strategies for isolated penetrating aortic ulcers (PAUs)

2020 ◽  
Vol 59 (5) ◽  
pp. e31
Author(s):  
Safa Salim ◽  
Rossella Locci ◽  
Guy Martin ◽  
Rick Gibbs ◽  
Michael Jenkins ◽  
...  
Keyword(s):  
Treatment Strategies ◽  
Long Term Outcomes ◽  
Short And Long Term

scholarly journals Does immunological remission, defined as disappearance of autoantibodies, occur with current treatment strategies? A long-term follow-up study in rheumatoid arthritis patients who achieved sustained DMARD-free status

2019 ◽  
Vol 78 (11) ◽  
pp. 1497-1504 ◽  
Author(s):  
Debbie M Boeters ◽  
Leonie E Burgers ◽  
René EM Toes ◽  
Annette van der Helm-van Mil
Keyword(s):  
Rheumatoid Arthritis ◽  
Treatment Strategies ◽  
Signs And Symptoms ◽  
Current Treatment ◽  
Dmard Therapy ◽  
Before And After ◽  
Long Term Follow Up ◽  
Free Status

ObjectivesSustained disease-modifying antirheumatic drug (DMARD)-free status, the sustained absence of synovitis after cessation of DMARD therapy, is infrequent in autoantibody-positive rheumatoid arthritis (RA), but approximates cure (ie, disappearance of signs and symptoms). It was recently suggested that immunological remission, defined as disappearance of anti-citrullinated protein antibodies (ACPA) and rheumatoid factor (RF), underlies this outcome. Therefore, this long-term observational study determined if autoantibodies disappear in RA patients who achieved sustained DMARD-free remission.MethodsWe studied 95 ACPA-positive and/or RF-positive RA patients who achieved DMARD-free remission after median 4.8 years and kept this status for the remaining follow-up (median 4.2 years). Additionally, 21 autoantibody-positive RA patients with a late flare, defined as recurrence of clinical synovitis after a DMARD-free status of ≥1 year, and 45 autoantibody-positive RA patients who were unable to stop DMARD therapy (during median 10 years) were studied. Anti-cyclic citrullinated peptide 2 (anti-CCP2) IgG, IgM and RF IgM levels were measured in 587 samples obtained at diagnosis, before and after achieving DMARD-free remission.Results13% of anti-CCP2 IgG-positive RA patients had seroreverted when achieving remission. In RA patients with a flare and persistent disease this was 8% and 6%, respectively (p=0.63). For anti-CCP2 IgM and RF IgM, similar results were observed. Evaluating the estimated slope of serially measured levels revealed that RF levels decreased more in patients with than without remission (p<0.001); the course of anti-CCP2 levels was not different (p=0.66).ConclusionsSustained DMARD-free status in autoantibody-positive RA was not paralleled by an increased frequency of reversion to autoantibody negativity. This form of immunological remission may therefore not be a treatment target in patients with classified RA.

scholarly journals Bilateral renal infarction with COVID-19 pneumonia: a case report

2021 ◽  
Vol 2021 (11-12) ◽  
Author(s):  
Kundan Jana ◽  
Kalyana C Janga ◽  
Sheldon Greenberg ◽  
Kamlesh Kumar
Keyword(s):  
Risk Factors ◽  
Acute Kidney Injury ◽  
Case Report ◽  
Young Patients ◽  
Treatment Strategies ◽  
Kidney Injury ◽  
Current Treatment ◽  
Renal Infarction ◽  
Patient Reported

ABSTRACT Acute renal infarction is a rare and often underdiagnosed condition with estimated incidence of 0.5–1.5%. Coronavirus disease 2019 (COVID-19) has been shown to cause a hypercoagulable state in patients leading to arterial and venous thromboembolism. Renal infarction as a consequence of COVID-associated coagulopathy has been reported, sometimes resulting in acute kidney injury. Most of the patients so far reported had other existing comorbidities and risk factors that compounded the risk of precipitating an infarction. Here, we present a 37-year-old, the youngest patient reported so far, with no pre-existing comorbidities or risk factors, who developed bilateral renal infarction with COVID-19 pneumonia. The patient was treated with anticoagulation for renal infarction and discharged on apixaban. Anticoagulation is an important part of current treatment strategies for COVID-19 pneumonia and should extend beyond the acute phase of the disease to prevent long-term sequelae, especially in young patients.

Ebola and Other Filoviruses

2018 ◽  
Author(s):  
Lisa M. Bebell
Keyword(s):  
Ebola Virus ◽  
Inflammatory Responses ◽  
Virus Disease ◽  
Treatment Strategies ◽  
Disease Outbreaks ◽  
Marburg Virus ◽  
Residual Effects ◽  
Long Term Outcomes ◽  
Pediatric Vaccination

Congenital and pediatric Ebola virus disease (EVD) and Marburg virus disease (MVD) are severe, even lethal infections. Historically, children have been underrepresented in filovirus disease outbreaks, and evidence-based treatment strategies are lacking. Existing data suggest that case fatalities are highest among children under four years of age, which is partially explained by higher virus concentrations in young children. Prevention and aggressive resuscitation, nutrition, and supportive care are the mainstays of management until filovirus-specific therapies can be developed. Differences in pediatric immune and inflammatory responses may necessitate unique approaches to pediatric vaccination and treatment. There are minimal safety or immunogenicity data in children, a crucial knowledge gap that must be addressed in future trials. Studying pediatric survivors of the 2014–2016 West Africa EVD outbreak will provide much-needed data on long-term outcomes and residual effects of filovirus disease while we await effective filovirus-specific vaccines and therapies.

Multiple Sclerosis

2017 ◽  
Author(s):  
Pavan Bhargava ◽  
Peter A. Calabresi
Keyword(s):  
Multiple Sclerosis ◽  
Immunosuppressive Agents ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Phase 2 ◽  
Future Directions ◽  
Disease Modifying Therapies ◽  
Future Challenges ◽  
Brain And Spinal Cord ◽  
The Brain

Multiple sclerosis is a chronic demyelinating neurological disorder of the brain and spinal cord, with both inflammatory and degenerative components. Current treatment strategies utilize immunomodulatory and immunosuppressive agents to reduce the inflammatory disease activity and retard accumulation of disability. Future challenges for treatment include identifying agents that will promote remyelination and axonal protection to help impact progressive forms of multiple sclerosis. This chapter discusses currently available disease modifying therapies, agents currently in phase 2/3 trials, and future directions in the treatment of multiple sclerosis.

scholarly journals Microglia: A Potential Therapeutic Target for Sepsis-Associated Encephalopathy and Sepsis-Associated Chronic Pain

2020 ◽  
Vol 11 ◽  
Author(s):  
Yi Li ◽  
Lu Yin ◽  
Zhongmin Fan ◽  
Binxiao Su ◽  
Yu Chen ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Immune Cell ◽  
Treatment Strategies ◽  
Neurological Dysfunction ◽  
Potential Therapeutic Target ◽  
The Central Nervous System ◽  
Underlying Mechanisms ◽  
The Relationship ◽  
The Brain

Neurological dysfunction, one of the severe manifestations of sepsis in patients, is closely related to increased mortality and long-term complications in intensive care units, including sepsis-associated encephalopathy (SAE) and chronic pain. The underlying mechanisms of these sepsis-induced neurological dysfunctions are elusive. However, it has been well established that microglia, the dominant resident immune cell in the central nervous system, play essential roles in the initiation and development of SAE and chronic pain. Microglia can be activated by inflammatory mediators, adjacent cells and neurotransmitters in the acute phase of sepsis and then induce neuronal dysfunction in the brain. With the spotlight focused on the relationship between microglia and sepsis, a deeper understanding of microglia in SAE and chronic pain can be achieved. More importantly, clarifying the mechanisms of sepsis-associated signaling pathways in microglia would shed new light on treatment strategies for SAE and chronic pain.

Antibody-Mediated Rejection and Lung Transplantation

2021 ◽  
Vol 42 (03) ◽  
pp. 428-435
Author(s):  
Laura P. Halverson ◽  
Ramsey R. Hachem
Keyword(s):  
Lung Transplantation ◽  
Diagnostic Criteria ◽  
Treatment Strategies ◽  
Current Treatment ◽  
Solid Organ ◽  
Term Survival ◽  
Antibody Mediated Rejection ◽  
History Of ◽  
Active Research

AbstractAntibody-mediated rejection (AMR) is now a widely recognized form of lung allograft rejection, with mounting evidence for AMR as an important risk factor for the development of chronic lung allograft dysfunction and markedly decreased long-term survival. Despite the recent development of the consensus diagnostic criteria, it remains a challenging diagnosis of exclusion. Furthermore, even after diagnosis, treatment directed at pulmonary AMR has been nearly exclusively derived from practices with other solid-organ transplants and other areas of medicine, such that there is a significant lack of data regarding the efficacy for these in pulmonary AMR. Lastly, outcomes after AMR remain quite poor despite aggressive treatment. In this review, we revisit the history of AMR in lung transplantation, describe our current understanding of its pathophysiology, discuss the use and limitations of the consensus diagnostic criteria, review current treatment strategies, and summarize long-term outcomes. We conclude with a synopsis of our most pressing gaps in knowledge, introduce recommendations for future directions, and highlight promising areas of active research.

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