Geriatric Neurology E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 2747

Veröffentlichungsjahr: 2014

Beschreibung

Aging affects neurological function leading to neurological disease As society grows older, so do the neurological problems associated with aging. These can be new neurological deficits due to the aging process itself, or the effect of aging on already existing neurological conditions. Neurologists will spend increasing amounts of time managing patients with age-related neurological complications. Geriatric Neurology brings together the wisdom of world-leading experts. They have crafted a new textbook to define this emerging subspecialty from basic science through clinical assessment and medical management to social aspects of patient care. Geriatric Neurology covers: * The aging brain in neurology * Assessment of the geriatric neurology patient * Neurological conditions in the elderly * Therapeutics for the geriatric neurology patient * Management issues beyond therapeutics Comprehensive in scope but with practical focus for effective patient care, Geriatric Neurology provides top-of-class guidance for the management of elderly patients with neurological disorders.

Leseprobe

I dedicate this book to my patients and mentors. This book would not be possible without my grandfather who carried me on his shoulders daily to an elementary school miles away and my very supportive family.

AKN

I dedicate this work to my mother and father, who nurtured my unquenchable thirst for knowledge.

MNS

Geriatric Neurology

EDITED BY

ANIL K. NAIR MD

Director, Clinic for Cognitive Disordersand Alzheimer’s Disease Center Chief of Neurology, Quincy Medical Center Quincy, MA, USA

MARWAN N. SABBAGH MD, FAAN

Director, Banner Sun Health Research Institute Research Professor of Neurology University of Arizona College of Medicine – Phoenix Sun City, AZ, USA

This edition first published 2014

© 2014 by John Wiley & Sons, Ltd

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Library of Congress Cataloging-in-Publication Data

Geriatric neurology (Nair)

Geriatric neurology/edited by Anil K. Nair and Marwan N. Sabbagh.

1 online resource.

Includes bibliographical references and index.

Description based on print version record and CIP data provided by publisher; resource not viewed.

ISBN 978-1-118-73064-5 (ePub) – ISBN 978-1-118-73065-2 (Adobe PDF) – ISBN 978-1-118-73068-3 (cloth)

I. Nair, Anil (Anil Kadoor), 1970- editor of compilation. II. Sabbagh, Marwan Noel, editor of compilation. III. Title.

[DNLM: 1. Nervous System Diseases. 2. Aged. 3. Aging–physiology. 4. Nervous System Physiological Phenomena. WL 140]

RC451.4.A5

618.97′68–dc23

2013038615

A catalogue record for this book is available from the British Library.

Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.

Cover images: top row - copyright Wiley; bottom - courtesy of Anil K. Nair

Cover design by Andy Meaden

CONTENTS

About the Editors

List of Contributors

Preface

Acknowledgements

Part 1 The Aging Brain in Neurology

1 The Biology of Aging: Implications for Diseases of Aging and Health Care in the Twenty-First Century

2 Functional Changes Associated with the Aging Nervous System

Part 2 Assessment of the Geriatric Neurology Patient

3 Approach to the Geriatric Neurology Patient: The Neurologic Examination

4 Assessment of Cognitive Status in Geriatric Neurology

4.1 Mental Status Examination in the Geriatric Neurology Patient

4.2 Neuropsychology in Geriatric Neurology

5 Cognitive Reserve and the Aging Brain

6 Gait Disorders in the Graying Population

7 Imaging of the Geriatric Brain

7.1 Structural Neuroimaging in Degenerative Dementias

7.2 Functional Imaging in Dementia

7.3 Amyloid Imaging

8 Clinical Laboratory Investigations in Geriatric Neurology

Part 3 Neurologic Conditions in the Elderly

9 Cognitive Impairment and the Dementias

9.1 Mild Cognitive Impairment

9.2 Alzheimer’s Disease

9.3 Dementia with Lewy Bodies

9.4 Vascular Cognitive Impairment

9.5 Frontotemporal Dementia

9.6 Primary Progressive Aphasia

9.7 Prion Diseases

9.8 Normal Pressure Hydrocephalus

10 Depression in the Elderly: Interactions with Aging, Stress, Chronic Pain, Inflammation, and Neurodegenerative Disorders

11 Cerebrovascular Diseases in Geriatrics

12 Movement Disorders

12.1 Parkinson’s Disease

12.2 Essential Tremor and Other Tremor Disorders

12.3 Progressive Supranuclear Palsy

12.4 Corticobasal Degeneration

13 Sleep Disorders

14 Autonomic Dysfunction and Syncope

15 Geriatric Epilepsy

16 Vertigo and Dizziness in the Elderly

17 Disorders of the Special Senses in the Elderly

18 Nervous System Infections

19 Delirium

20 Headache in the Elderly

21 Neuromuscular Disorders

Part 4 Therapeutics for the Geriatric Neurology Patient

22 Neurosurgical Care of the Geriatric Patient

23 Treatment of Dementia

23.1 Evidence-Based Pharmacologic Treatment of Dementia

23.2 Immunotherapy for Alzheimer’s Disease

24 Geriatric Psychopharmacology

25 Nonpharmacologic Treatment of Behavioral Problems in Persons with Dementia

26 Expressive Art Therapies in Geriatric Neurology

Part 5 Important Management Issues Beyond Therapeutics in the Geriatric Neurology Patient

27 Dietary Factors in Geriatric Neurology

28 Exercising the Brain: Nonpharmacologic Interventions for Cognitive Decline Associated with Aging and Dementia

29 Driving Impairment in Older Adults

30 Elder Abuse and Mistreatment

31 Advocacy in Geriatric Neurology

Index

List of Tables

Chapter 1

Table 1.1

Chapter 3

Table 3.1

Table 3.2

Table 3.3

Chapter 4

Table 4.1

Table 4.2

Table 4.3

Table 4.1

Table 4.2

Table 4.3

Chapter 6

Table 6.1

Chapter 7

Table 7.1

Chapter 8

Table 8.1

Table 8.2

Table 8.3

Chapter 9

Table 9.1

Table 9.2

Table 9.3

Table 9.4

Table 9.5

Table 9.6

Table 9.7

Table 9.8

Table 9.9

Table 9.10

Table 9.11

Table 9.12

Table 9.13

Table 9.14

Table 9.15

Chapter 10

Table 10.1

Chapter 11

Table 11.1

Table 11.2

Table 11.3

Table 11.4

Chapter 12

Table 12.1

Table 12.2

Table 12.3

Chapter 14

Table 14.1

Table 14.2

Chapter 16

Table 16.1

Table 16.2

Table 16.3

Table 16.4

Table 16.5

Chapter 17

Table 17.1

Table 17.2

Chapter 18

Table 18.1

Table 18.2

Table 18.3

Table 18.4

Table 18.5

Table 18.6

Table 18.7

Table 18.8

Chapter 19

Table 19.1

Table 19.2

Table 19.3

Chapter 22

Table 22.1

Chapter 23_1

Table 23.1

Table 23.2

Table 23.3

Table 23.4

Table 23.5

Table 23.6

Table 23.7

Table 23.8

Table 23.9

Table 23.10

Chapter 24

Table 24.1

Table 24.2

Table 24.3

Table 24.4

Table 24.5

Table 24.6

Table 24.7

Table 24.8

Table 24.9

Table 24.10

Table 24.11

Table 24.12

Table 24.13

Table 24.14

Table 24.15

Chapter 30

Table 30.1

Table 30.2

Table 30.3

List of Illustrations

Chapter 1

Figure 1.1

Cell cycle factors related to aging based on the stochastic acceleration hypothesis of Collier, Kanaan & Kordower (2011). A revised hypothesis of the relationship between aging and Parkinson’s disease (PD) as they affect the biology of midbrain dopamine (DA) neurons. The hypothesis incorporates evidence that supports the involvement of common cellular mechanisms in dopamine neuron dysfunction in ageing and degeneration in Parkinson’s disease. (a) The effects of these altered cellular mechanisms as they accumulate during normal ageing result in Parkinsonian dopamine neuron dysfunction, either very late in life or not at all (shown by the light gray line). However, when these same cellular mechanisms are accelerated by specific, individually determined factors, Parkinsonism emerges earlier in the lifespan (shown by the dark gray line). (b) The hypothesis contends that the cellular mechanisms that threaten dopamine neuron function are identical, but are not linked in an orderly cascade of cause and effect; instead, they can contribute to varying degrees and combine in patient-specific patterns, thus fulfilling the definition of a stochastic interaction: incorporating elements of randomness with directionality toward dopamine neuron dysfunction. Light gray double-ended arrows show cellular events in normal ageing. Thicker, dark gray double-ended arrows show accelerated cellular events in PD. UPS, ubiquitin-proteasome system. Similar mechanisms are implicated in cancer pathogenesis also.

Source:

Blagosklonny (2011). Reproduced with permission from US Administration on Aging.

Figure 1.2

A simple schematic for the molecular pathway of mTOR as “antagonistic pleiotropy”–that, in some sense, aging is simply the flip side of a protracted growth process that is not sufficiently turned off after a peak reproductive period.

Source:

Blagosklonny (2009). Reproduced with permission from US Administration on Aging.

Figure 1.3

A simple schematic of some of the cellular pathways implicated in calorie restriction, aging, and the slowing of aging. Nutrients, growth factors (GF), and insulin activate the TOR pathway, which is involved in aging and age-related diseases. Other genetic factors and environmental factors (such as smoking, sedentary lifestyles, and obesity) contribute to age-related diseases. Several potential antiaging modalities (metformin, calorie restriction, and rapamycin and several polyphenols particularly resveratrol) all directly or indirectly (via impact on AMP kinase) inhibit the TOR pathway.

Source:

Blagosklonny (2009, 2010a). Reproduced with permission from US Administration on Aging.

Figure 1.4

A schematic summarizing the hypothesis for how diet balance might affect lifespan via the TOR and AMPK signaling pathways.

Source:

Simpson and Raubenheimer (2009). Reproduced with permission from US Administration on Aging.

Chapter 2

Figure 2.1

Apical dendrite (arrow head) and cell body (arrow) of pyramidal neuron, hippocampus CA1, mouse brain (Golgi stain).

Figure 2.2

Dendritic spines, mouse brain, hippocampus CA1 (Golgi stain).

Figure 2.3

Activated cortical microglia in older person without cognitive impairment; antibody to class II major histocompatibility antigen (MHCII).

Figure 2.4

Alzheimer’s disease brain showing (a) narrowing of gyri and widened sulci, and hippocampal atrophy with enlargement of lateral ventricles, especially temporal horn (b).

Figure 2.5

Neurofibrillary tangles: (a) hippocampus CA1 (modified Bielschowsky stain); (b) frontal cortex (immunohistochemistry with antibodies to paired helical filament).

Figure 2.6

Ghost tangles, hippocampus CA1 (modified Bielschowsky silver stain).

Figure 2.7

Neuritic plaque pathology in AD. (a) Three NPs in the neocortex on H&E stain are difficult to see. (b) The same NPs are easily visualized on modified Bielschowsky silver stain.

Figure 2.8

Amyloid pathology in AD. (a) Numerous amyloid immunostained plaques in the cortex at low power. (b) Leptomeningeal arterioles also may show amyloid deposition. (c, d) Higher power of plaque pathology using amyloid immunostain.