The Social Security Administration (SSA) uses a screening tool called the Listing of Impairments to identify claimants who are so severely impaired that they cannot work at all and thus immediately qualify for benefits. In this report, the IOM makes several recommendations for improving SSA's capacity to determine disability benefits more quickly and efficiently using the Listings.

Over the past decade, the hospitalist model has become a dominant system for the delivery of inpatient care. Forces such as national mandates to improve safety and quality, and intense pressure to safely reduce length of hospital stays, are now exerting pressure on neurologists. To meet these challenges, a new neurohospitalist model is emerging. This is the first authoritative text to detail the advances and strategies for treating neurologic disease in a hospital setting. It includes chapters on specific acute neurologic diseases including stroke, epilepsy, neuromuscular disease and traumatic brain injury and also addresses common reasons for neurologic consultation in the hospital including encephalopathy, electrolyte disturbances and neurologic complications of pregnancy. Ethical and structural issues commonly encountered in neurologic inpatients are also addressed. This will be a key resource for any clinician or trainee caring for neurologic patients in the hospital including practising neurologists, internists and trainees across multiple subspecialities.

New updated edition first published with Cambridge University Press. This new edition includes 29 chapters on topics as diverse as pathophysiology of atherosclerosis, vascular haemodynamics, haemostasis, thrombophilia and post-amputation pain syndromes.

A distinction between primary and secondary brain damage of vari ous origin, particularly in acute lesions, such as head injury and ische mia is not entirely new. The concept is of practical significance, be cause it is the foremost intention of all clinical efforts to prevent, or at least attenuate the development of secondary sequelae. Primary dam age to nervous elements usually cannot be influenced by treatment. Its prevention is the objective of prophylactic measures. The current volume gathered prominent scientists and clinicians from various fields to pro vide a competent introduction and survey of the various aspects involved in secondary brain damage. It was attempted to provide criteria for the distinction between the primary and secondary phenomena on a morpho logical and functional level, on the basis of the kinetics involved and, most importantly, regarding the different specific manifestations, such as disturbances of microcirculation, aspects of the blood-brain barrier, and of cellular structure and function at a molecular level. Although it was not expected that a grand unifying hypothesis will be reached recon cilable with the many, occasionally opposing views on such a complex subject, nevertheless, the present volume attains an appropriate result. It can best be described as a mosaic of many different pieces which only as an ensemble reflect the current state of the art.

This updated second edition of Acute Ischemic Stroke: Imaging and Intervention provides a comprehensive account of the state of the art in the diagnosis and treatment of acute ischemic stroke. The basic format of the first edition has been retained, with sections on fundamentals such as pathophysiology and causes, imaging techniques and interventions. However, each chapter has been revised to reflect the important recent progress in advanced neuroimaging and the use of interventional tools. In addition, a new chapter is included on the classification instruments for ischemic stroke and their use in predicting outcomes and therapeutic triage. All of the authors are internationally recognized experts and members of the interdisciplinary stroke team at the Massachusetts General Hospital and Harvard Medical School. The text is supported by numerous informative illustrations, and ease of reference is ensured through the inclusion of suitable tables. This book will serve as a unique source of up-to-date information for neurologists, emergency physicians, radiologists and other health care providers who care for the patient with acute ischemic stroke.

Development of the brain and the emergence of the mind constitute some of the most important concerns of contemporary biology. Disturbances during fetal life may have profound implications for a child's future neurological and psychological development, which can in turn impact society. The new edition of this highly respected work presents a comprehensive review of the basic mechanisms of brain development and the pathophysiology of disorders of the infant brain, written by a team of distinguished neuroscientists, neonatologists, and neuropediatricians. The book follows the main milestones of brain development, from formation of the neural tube and wiring of the neurons in the brain. Neurotrophic factors, neurotransmitters, glial cell biology, cerebral circulation development of sensory functions are all described in detail. Furthermore, there are more philosophical chapters on the evolution of the brain and the emergence of consciousness. Clinical considerations are highlighted where relevant.

The World Stroke Organization reports that “stroke has already reached epidemic proportions. Globally1 in 4 adults over the age of 25 will have a stroke in their lifetime. 12.2 million people worldwide will have their first stroke this year, and 6.5 million will die as a result.” Ischemic strokes are the most common type of stroke, with about 87% of all strokes being ischemic strokes. This new volume addresses this epidemic by presenting detailed studies on ischemic injury, with emphasis on the molecular-level mechanisms and the role of signaling pathways in the body, their structure, and their mechanism of action. The book focuses on molecular pharmacology plans and explains the new areas of research on the discovery of therapeutic molecules that can be used for combating this life-threatening disease. The authors discuss stroke occurrence at different stages of life as well as sex-based differences in its treatment. They cover aspects of the clinical treatment and diagnosis of patients with cardiovascular events, including in-depth information on the prevention, evaluation, therapy selection, result projection, and long-term course of the disease in affected patients. They also detail the involvement of platelets, neurotransmitters, renin-angiotensin-aldosterone system, and vitamin D in ischemic injury.

The human brain represents about 2% of the body weight, yet it accounts for approximately 20% of aerobic metabolism. This high dependency on energy-consuming processes is mainly caused by the active transport of ions, which is necessary to compensate for the transmembrane ion currents that are part ofthe complex signaling processes in the brain. Ninety-five percent ofthe brain's ATP is derived from mitochondrial oxidative phosphorylation. Since that organ' s storage capacity for oxygen is minimal, any interruption of oxygen delivery to brain cells willlead to changes in membrane excitability and, there fore, to disruption of neuronal signaling within seconds. It seems that mamma lian brain is especially vulnerable to such an interruption, since oxygen deprivation leads to activation of ion channel mechanisms in neurons that impair their communications. Thus, the function of the brain as a coordinator of vital homeostatic reflexes, and complex body reactions to external challenges, depends critically on the rate of oxygen delivery and oxygen consumption. Oxygen delivery depends on two variables described in the Fick relation ship: volume flow rate ofblood and the arterial oxygen content. A reduction in either of these two variables will have serious effects on vital brain func tions. Reduction of arterial blood flow to the brain can be caused by cardiac arrest, shock, carotid occlusion, Of hypotension (global ischemia). Oxygen content is progressively decreased in asphyxia (including drowning).

The microcirculation of the gastrointestinal tract is under the control of both myogenic and metabolic regulatory systems. The myogenic mechanism contributes to basal vascular tone and the regulation of transmural pressure, while the metabolic mechanism is responsible for maintaining an appropriate balance between O2 demand and O2 delivery. In the postprandial state, hydrolytic products of food digestion elicit a hyperemia, which serves to meet the increased O2 demand of nutrient assimilation. Metabolically linked factors (e.g., tissue pO2, adenosine) are primarily responsible for this functional hyperemia. The fenestrated capillaries of the gastrointestinal mucosa are relatively permeable to small hydrolytic products of food digestion (e.g., glucose), yet restrict the transcapillary movement of larger molecules (e.g., albumin). This allows for the absorption of hydrolytic products of food digestion without compromising the oncotic pressure gradient governing transcapillary fluid movement and edema formation. The gastrointestinal microcirculation is also an important component of the mucosal defense system whose function is to prevent (and rapidly repair) inadvertent epithelial injury by potentially noxious constituents of chyme. Two pathological conditions in which the gastrointestinal circulation plays an important role are ischemia/reperfusion and chronic portal hypertension. Ischemia/reperfusion results in mucosal edema and disruption of the epithelium due, in part, to an inflammatory response (e.g., increase in capillary permeability to macromolecules and neutrophil infiltration). Chronic portal hypertension results in an increase in gastrointestinal blood flow due to an imbalance in vasodilator and vasoconstrictor influences on the microcirculation. Table of Contents: Introduction / Anatomy / Regulation of Vascular Tone and Oxygenation / Extrinsic Vasoregulation: Neural and Humoral / Postprandial Hyperemia / Transcapillary Solute Exchange / Transcapillary Fluid Exchange / Interaction of Capillary and Interstitial Forces / Gastrointestinal Circulation and Mucosal Defense / Gastrointestinal Circulation and Mucosal Pathology I: Ischemia/Reperfusion / Gastrointestinal Circulation and Mucosal Pathology II: Chronic Portal Hypertension / Summary and Conclusions / References / Author Biography

Brain Hypoxia and Ischemia explores the various aspects of cell death and survival that are crucial for understanding the basic mechanisms underlying brain hypoxia and ischemia. Chapters focus on a panorama of issues including the role of ion channels/transporters, mitochondria and apoptotic mechanisms, the roles of glutamate/NMDA, mechanisms in penumbral cells and the importance of intermittent hypoxia and gene regulation under these stressful conditions. The volume explores findings from both mammalian and invertebrate model systems and their applicability to human systems and diseases. Careful consideration is also given to differences in hypoxia and ischemia across development. This volume aims to increase the understanding of these mechanisms and to stimulate research on better diagnosis and treatment of diseases that afflict the brain and potentially other organs when O2 levels are dysregulated. Brain Hypoxia and Ischemia is designed for neuroscientists, clinicians and medical/graduate students for use in both basic research and clinical practice.