Vol 2-1 Mini Review

Decompressive Hemicraniectomy for Stroke in Older Adults: A Review

Faith C. Robertson B.S.,1,2 Hormuzdiyar H. Dasenbrock M.D., M.P.H.,1,2,3 William B. Gormley M.D., M.P.H., M.B.A.1,2,3

1Harvard Medical School, Boston, Massachusetts, USA
2Cushing Neurosurgical Outcomes Center, Brigham and Women's Hospital, Boston, Massachusetts, USA
3Department of Neurological Surgery, Brigham and Women's Hospital, Boston, Massachusetts, USA

Malignant cerebral edema is a potential consequence of large territory cerebral infarction, as the resultant elevation in intracranial pressure may progress to transtentorial herniation, brainstem compression, and death. In appropriate patients, decompressive hemicraniectomy (DHC) reduces mortality without increasing the risk of severe disability. However, as the foundational DHC randomized, controlled trials excluded patients greater than 60 years of age, the appropriateness of DHC in older adults remains controversial. Recent clinical trials among elderly participants, including DESTINY II, reported that DHC reduces mortality, but may leave patients with substantial morbidity. Nationwide analyses have demonstrated generalizability of such data. However, what constitutes an acceptable outcome − the perspective on quality of life after survival with substantial disability − varies between clinicians, patients, and caregivers. Consequently, quality of life measures are being increasingly incorporated into stroke research. This review summarizes the impact of DHC in space-occupying cerebral infarction, and the influence of patient age on postoperative survival, functional capacity, and quality of life-all key factors in the clinical decision process. Ultimately, these data underscore the inherent complexity in balancing scientific evidence, clinical expertise, and patient and family preference when pursuing hemicraniectomy among the elderly.

Abbreviations: BI: Barthel Index; DHC: decompressive hemicraniectomy; EQ-5D: European Quality of Life Scale; mRS: modified Rankin Scale; QoL: quality of life; RCT: randomized controlled trial.

DOI: 10.29245/2572.942X/2017/2.942X/2017/1.1103 View / Download Pdf
Vol 2-1 Mini Review

Alzheimer's and cerebrovascular disease: the twin towers of dementia.

Joel Ramireza-b, Melissa F. Holmesa, Fuqiang Gaoa-b, and Sandra E. Blacka-c

aLC Campbell Cognitive Neurology Research Unit, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada
bHeart & Stroke Foundation Canadian Partnership for Stroke Recovery, Toronto, Ontario, Canada
cDepartment of Medicine (Neurology), University of Toronto and Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada.

With dementia prevalence on the rise, it is imperative to develop novel therapies and treatments to address the increasing recognition of the clinical and pathological overlap of Alzheimer’s and cerebrovascular disease - the top two leading causes of dementia. Although the research methods currently employed have made great advances towards our understanding of comorbid neurovascular and neurodegenerative diseases, these knowledge-based silos have had a tendency to operate in relative isolation. As our cumulative body of knowledge within each platform increases, so should the coordination of research. By examining current findings in neuroimaging, neuropsychology, genetics, neuropathology, and molecular neurobiology, this blanket-level mini-review will examine the spectrum of research findings that contributes to our understanding of Alzheimer’s and vascular contributions to dementia.

DOI: 10.29245/2572.942X/2017/1.1105 View / Download Pdf
Vol 2-1 Mini Review

The two sides of Faim2 -- modulation of cell death and regeneration

Björn Falkenburger and Arno Reich

Department of Neurology, RWTH Aachen University, Aachen, Germany

DOI: 10.29245/2572.942X/2017/2.942X/2017/1.1101 View / Download Pdf
Vol 2-1 Mini Review

Neuroinflammation and Mitochondrial Dysfunction in the Pathogenesis of Alzheimer's Disease: Modulation by Coriolus Versicolor (Yun-Zhi) Nutritional Mushroom

Angela Trovato1, Manuela Pennisi1,5, Rosalia Crupi2*, Rosanna Di Paola2, Alice Alario1, Sergio Modafferi1, Gabriele Di Rosa1, Tito Fernandes3, Anna Signorile4, Luigi Maiolino6, Salvatore Cuzzocrea2 and Vittorio Calabrese1**

1Department of Biomedical and Biotechnological Sciences, School of Medicine, University of Catania, Catania, Italy
2Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy
3Faculty of Veterinary Medicine, Lisbon University, Portugal
4Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari, Bari, Italy
5Spinal Unit, Emergency Hospital "Cannizzaro", Catania, Italy

Abnormal redox homeostasis and oxidative stress have been proposed to play a role in the etiology of several neuropsychiatric disorders and emerging interest has recently focused on markers of oxidative stress and neuroinflammation in neurodegenerative disorders as well as in different forms of chronic mental illness. Oxidative stress and altered antioxidant systems have been considered an important factor underlying the pathogenesis of Alzheimer’s disease (AD). Altered expression of genes related to oxidative stress, oxidative damage to DNA, protein and lipids, as well as alterations in the redox state in central and peripheral tissues could act synergistically, and contribute to the course of the disease. Specifically, we discuss the emerging role of lipoxinA4 and inflammasome in neurodegeneration. However, the notion that low levels of stress can induce responses that may be protective against the pathogenic processes is a frontier area of neurobiological research focal to understanding and developing therapeutic approaches to neurodegenerative disorders. Herein, we discuss the potenial therapeutic role of Coriolus versicolor, a mushrooom, well known in China as Yun Zhi. We propose a potentially innovative treatment for AD and, possibly, other neurodegenerative conditions associated to neuroinflammation.

DOI: 10.29245/2572.942X/2017/2.942X/2017/1.1088 View / Download Pdf