Neuroscience Nursing E-Book
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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
"Superior... An important resource for nurses" Shanne McNamara, Vice President, British Association of Neuroscience Nurses Neuroscience Nursing is a comprehensive, practical text that reflects both the richness and the diversity of contemporary neuroscience nursing. It aims to inform the practice of neuroscience nursing through the report of current research, best available evidence, policy and education. This important new book is divided into several sections exploring anatomy and physiology of the nervous system; assessment, interpretation and management of specific problems in the neurological patient; neurological investigations and neurosurgical procedures; management of patients with intracranial disorders; and management of patients with long-term conditions. It also explores the underpinning concepts of neuroscience care, including its history and development, and legal and ethical issues. Uniquely, this text also includes patients' perspectives of living with a variety of neurological conditions. Key features: * The first evidence-based UK neuroscience textbook for nurses * Extensive full colour illustrations throughout * Applicable to a wide variety of settings including prevention, primary care, acute and critical care, rehabilitation and palliative care * Contributions from nurse specialists, nurse consultants, academics and subject experts from throughout the UK
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Veröffentlichungsjahr: 2010
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Table of Contents
Cover
Table of Contents
Half title page
Title page
Copyright page
Contributor List
Preface
Acknowledgements
Section I: Anatomy and Physiology of the Nervous System
1 Cells of the CNS and How They Communicate
INTRODUCTION
COMPONENTS OF THE NEURONE AND THEIR FUNCTIONS
NEUROGLIA
COMMUNICATION BY NEURONES
NEUROTRANSMISSION
SUMMARY
2 The Structural and Biochemical Defences of the CNS
INTRODUCTION
BONY ENCASEMENT
THE MENINGES AND CEREBROSPINAL FLUID (CSF)
BLOOD SUPPLY TO THE CNS
THE BLOOD–BRAIN BARRIER (BBB)
SUMMARY
3 The Anatomy and Physiology of the Brain
INTRODUCTION
DESCRIBING ANATOMICAL STRUCTURES
FOETAL DEVELOPMENT OF THE BRAIN
THE GROSS ANATOMY OF THE BRAIN
CEREBRUM
FRONTAL LOBE
PARIETAL LOBE
TEMPORAL LOBE
OCCIPITAL LOBE
LIMBIC SYSTEM
AMYGDALA
HIPPOCAMPUS AND MEMORY
MAMILLARY BODIES
SEPTUM PELLUCIDUM
CINGULATE GYRUS, INSULA AND PARAHIPPOCAMPAL GYRUS
CEREBELLUM
BASAL GANGLIA AND THE THALAMUS
THE HYPOTHALAMUS
PITUITARY GLAND (HYPOPHYSIS)
BRAIN STEM
RETICULAR FORMATION AND RETICULAR ACTIVATING SYSTEM
SUMMARY
4 The Spinal Cord
INTRODUCTION
GROSS ANATOMY
PHYSIOLOGY
SUMMARY
5 The Autonomic Nervous System
INTRODUCTION
ANATOMY
NEUROTRANSMITTERS AND RECEPTORS
THE SENSORY COMPONENT
THE ENTERIC NERVOUS SYSTEM
VISCERAL PAIN
THE FUNCTION OF THE AUTONOMIC NERVOUS SYSTEM
THE HYPOTHALAMUS
THE AUTONOMIC NERVOUS SYSTEM, EMOTION AND THE CONSCIOUS BRAIN
SUMMARY
6 Intracranial Physiology
INTRODUCTION
INTRACRANIAL PRESSURE
CEREBRAL BLOOD FLOW (CBF)
OXYGEN AND GLUCOSE REQUIREMENTS
SUMMARY
Section II: Assessment, Interpretation and Management of Specific Problems in the Neurological Patient
7 Assessment and Management of Raised Intracranial Pressure
INTRODUCTION
CAUSES OF RAISED ICP
SIGNS AND SYMPTOMS
INVESTIGATIONS
ASSESSMENT
TREATMENT OF RAISED ICP
GENERAL MEASURES AND NURSING CARE FOR PATIENTS WITH RAISED ICP OR SUSPECTED RAISED ICP
FIRST LINE MEASURES TO REDUCE ICP
SUMMARY
8 Assessment, Interpretation and Management of Altered Consciousness
INTRODUCTION
CONSCIOUSNESS
SLEEP
ASSESSMENT OF CONSCIOUSNESS
INTERPRETATION OF GCS FINDINGS
ALTERED STATES OF CONSCIOUSNESS
BRAIN STEM DEATH
NURSING MANAGEMENT OF A PATIENT WITH ALTERED CONSCIOUSNESS
NURSING MANAGEMENT OF A PATIENT WITH BRAIN STEM DEATH
SUMMARY
9 Assessment, Interpretation and Management of Impaired Cognition
INTRODUCTION
PHYSIOLOGY OF COGNITION
PATHOPHYSIOLOGY AND ALTERED COGNITION
AETIOLOGY AND PRESENTATION OF DELIRIUM
ASSESSING PATIENTS WITH IMPAIRED COGNITION
INTERPRETATION OF ASSESSMENT FINDINGS
NURSING MANAGEMENT OF DELIRIUM
MULTIDISCIPLINARY TEAMWORKING
POST-DELIRIUM COUNSELLING
SUMMARY
10 Assessment and Management of Challenging Behaviour
INTRODUCTION
PATHOPHYSIOLOGY
EPIDEMIOLOGY
ASSESSMENT
MANAGEMENT
ENVIRONMENTAL AND BEHAVIOURAL MANAGEMENT STRATEGIES
STAFF INTERACTIONS AND BEHAVIOURS
PHARMACOLOGICAL MANAGEMENT
PHYSICAL RESTRAINT
SUMMARY
11 Assessment, Interpretation and Management of Altered Perceptual, Motor and Sensory Function
INTRODUCTION
SENSATION
SENSORY ASSESSMENT
SENSORY IMPAIRMENT
PHYSIOLOGY OF MOVEMENT
ASSESSMENT OF MOVEMENT
ABNORMAL MOVEMENTS AND MOVEMENT DISORDERS
SPASTICITY, RIGIDITY AND CONTRACTURE
NURSING CARE OF THE PATIENT WITH MOTOR IMPAIRMENT
SPECIFIC NURSING MANAGEMENT OF SPASTICITY
SPECIFIC NURSING MANAGEMENT OF FLACCIDITY
SUMMARY
12 Assessment, Interpretation and Management of Altered Speech and Swallowing
INTRODUCTION
OVERVIEW OF ALTERED SPEECH
THE ASSESSMENT AND INTERPRETATION OF COMMUNICATION
ASSESSMENT OF COMMUNICATION
NURSING MANAGEMENT OF ALTERED COMMUNICATION
MEDICAL MANAGEMENT RELATED TO ALTERED COMMUNICATION
OVERVIEW OF ALTERED SWALLOWING (DYSPHAGIA)
AETIOLOGY OF NEUROGENIC DYSPHAGIA
ASSESSMENT OF DYSPHAGIA
NURSING MANAGEMENT OF DYSPHAGIA
SUMMARY
13 Assessment, Interpretation and Management of Cranial Nerve Dysfunction
INTRODUCTION
FUNCTIONS OF THE CRANIAL NERVES
TESTING CRANIAL NERVES AND INTERPRETING FINDINGS
CRANIAL NERVE DISORDERS
MEDICAL AND NURSING MANAGEMENT OF COMMON CRANIAL NERVE DISORDERS
SUMMARY
14 Assessment, Interpretation and Management of Altered Cardiovascular Status in the Neurological Patient
INTRODUCTION
HAEMODYNAMICS
AUTONOMIC CONTROL OF HAEMODYNAMICS
HAEMODYNAMIC ASSESSMENT
TEMPERATURE
HAEMODYNAMIC EFFECTS OF NERVOUS SYSTEM DISEASE
BRAIN STEM DEATH
AUTONOMIC EFFECTS OF PERIPHERAL NERVE DISEASE
TEMPERATURE ABNORMALITIES AND NERVOUS SYSTEM DISEASE
SUMMARY
15 Assessment, Interpretation and Management of Impaired Respiratory Function in the Neurological Patient
INTRODUCTION
PHYSIOLOGY
ASSESSMENT OF RESPIRATORY FUNCTION
MONITORING AND INVESTIGATION OF RESPIRATORY FUNCTION
ACID–BASE BALANCE
DISTURBANCES OF ACID–BASE BALANCE
NURSING CARE/MANAGEMENT
RESPIRATORY SUPPORT
NON-INVASIVE RESPIRATORY SUPPORT
SUCTIONING
ASSISTED COUGH
SUMMARY
16 Assessment and Management of Fluid, Electrolytes and Nutrition in the Neurological Patient
INTRODUCTION
PHYSIOLOGY OF FLUID AND ELECTROLYTE BALANCE
FLUID ASSESSMENT IN THE NEUROSCIENCE PATIENT
FLUID MANAGEMENT
MANAGEMENT OF COMMON CAUSES OF HYPONATRAEMIA IN THE NEUROLOGICAL PATIENT
MANAGEMENT OF COMMON CAUSES OF HYPERNATRAEMIA IN THE NEUROLOGICAL PATIENT
NUTRITION IN THE NEUROSCIENCE PATIENT
BIOCHEMICAL AND PHYSICAL ASSESSMENT
MECHANISMS OF NUTRITIONAL SUPPORT
SUMMARY
17 Assessment and Management of Pain
INTRODUCTION
DEFINING PAIN
PHYSIOLOGY OF PAIN
SOMATIC AND VISCERAL PAIN
NEUROPATHIC PAIN
ASSESSMENT OF PAIN
HEADACHE
MEDICAL AND NURSING MANAGEMENT OF PAIN
MANAGEMENT OF HEADACHE
MANAGEMENT OF NEUROPATHIC, SOMATIC AND VISCERAL PAIN
SUMMARY
18 Assessment and Management of Bladder and Bowel Problems
INTRODUCTION
PHYSIOLOGY OF MICTURITION
URINARY SYMPTOMS AND INCONTINENCE
NEUROLOGICAL CONDITIONS AND BLADDER DYSFUNCTION
ASSESSMENT OF BLADDER FUNCTION
MEDICAL AND NURSING MANAGEMENT OF URINARY INCONTINENCE
PHYSIOLOGY OF DEFECATION
NEUROLOGICAL CONDITIONS AND BOWEL DISORDERS
ASSESSING BOWEL FUNCTION
BOWEL MANAGEMENT PROGRAMMES
SUMMARY
Section III: Neurological Investigations and Neurosurgical Procedures
19 Neurological Investigations
INTRODUCTION
STRUCTURAL NEUROIMAGING: CRANIAL STRUCTURES
STRUCTURAL NEUROIMAGING: SPINAL STRUCTURES
FUNCTIONAL NEUROIMAGING
NEUROPHYSIOLOGY
BIOPSIES
LUMBAR PUNCTURE (LP)
SUMMARY
20 Common Neurosurgical Procedures
INTRODUCTION
GENERAL PRE-OPERATIVE NURSING MANAGEMENT
IMMEDIATE PRE-OPERATIVE PREPARATION
OVERVIEW OF SURGICAL PROCEDURES
POST-OPERATIVE NURSING MANAGEMENT FOR ALL NEUROSURGICAL PATIENTS
SPECIFIC POST-OPERATIVE NEUROSURGICAL NURSING CARE
SUMMARY
Section IV: Management of Patients with Intracranial Disorders and Disease
21 Management of Patients with Intracranial Tumours
INTRODUCTION
EPIDEMIOLOGY
PATHOPHYSIOLOGY
AETIOLOGY
OVERVIEW OF TUMOUR TYPES AND CLASSIFICATION
COMMON TYPES OF TUMOUR: GLIOMA, MENINGIOMA AND METASTASES
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
TREATMENT
SPECIFIC TREATMENT FOR EACH TYPE OF TUMOUR
LESS COMMON TYPES OF TUMOUR
PITUITARY TUMOURS
FUNCTIONING PITUITARY TUMOURS
NON-FUNCTIONING PITUITARY TUMOURS
RARE TUMOURS INVOLVING THE PITUITARY GLAND
VESTIBULAR SCHWANNOMA – ACOUSTIC NEUROMA
RARE TUMOURS: INCIDENCE OF LESS THAN 1–2 PER MILLION PER YEAR
SERVICE GUIDANCE FOR THE MANAGEMENT OF PATIENTS WITH BRAIN TUMOURS
NURSING CARE AND MANAGEMENT
CARE OF THE PATIENT UNDERGOING RADIOTHERAPY
CARE OF THE PATIENT UNDERGOING CHEMOTHERAPY
CARE OF THE PATIENT UNDERGOING STEROID THERAPY
SUMMARY
22 Management of Patients with Stroke and Transient Ischaemic Attack
INTRODUCTION
DEFINITIONS
EPIDEMIOLOGY
AETIOLOGY
RISK FACTORS
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS OF STROKE
DIAGNOSIS
MEDICAL MANAGEMENT OF STROKE AND TIA
SURGICAL MANAGEMENT OF STROKE AND TIA
EVIDENCE-BASED NURSING MANAGEMENT
STROKE REHABILITATION
SUMMARY
23 Management of Patients with Intracranial Aneurysms and Vascular Malformations
INTRODUCTION
ANEURYSMS
INCIDENCE OF ANEURYSMS
AETIOLOGY OF ANEURYSMS
OTHER CAUSES OF SPONTANEOUS SUBARACHNOID HAEMORRHAGE (SAH)
SIGNS AND SYMPTOMS OF ANEURYSMAL SAH
DIAGNOSIS
NURSING AND MEDICAL MANAGEMENT OF THE PATIENT WITH AN ANEURYSMAL SAH
EXTRACRANIAL COMPLICATIONS ASSOCIATED WITH SAH
TREATMENT OF THE ANEURYSM
SPECIFIC NURSING MANAGEMENT TO MONITOR/TREAT FOR POST-COILING COMPLICATIONS
PROGNOSTIC FACTORS
OUTCOMES
ARTERIOVENOUS MALFORMATIONS
INCIDENCE
AETIOLOGY
PRESENTATION SIGNS AND SYMPTOMS
TREATMENT
NURSING MANAGEMENT
OUTCOMES
OTHER VASCULAR MALFORMATIONS
SUMMARY
24 Management of Patients with Central Nervous System Infections
ACUTE BACTERIAL MENINGITIS
AETIOLOGY AND EPIDEMIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT AND TREATMENT
NURSING MANAGEMENT
TRANSMISSION
PROGNOSIS
PHYSICAL, COGNITIVE AND PSYCHOSOCIAL IMPAIRMENTS FOLLOWING MENINGITIS
SUPPORT
SUBACUTE MENINGITIS
ENCEPHALITIS
EPIDEMIOLOGY AND AETIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
PROGNOSIS
PHYSICAL, COGNITIVE AND PSYCHOSOCIAL IMPAIRMENTS FOLLOWING ENCEPHALITIS
FURTHER INFORMATION
CEREBRAL ABSCESS
AETIOLOGY AND EPIDEMIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS AND MEDICAL MANAGEMENT
NURSING MANAGEMENT
PROGNOSIS
NEUROLOGICAL COMPLICATIONS OF HUMAN IMMUNODEFICIENCY VIRUS (HIV)
EPIDEMIOLOGY OF HIV
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS AND INVESTIGATIONS
MEDICAL MANAGEMENT AND DRUGS
NURSING MANAGEMENT
SUMMARY
25 Management of Patients with Hydrocephalus
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY AND PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
INVESTIGATIONS
TREATMENT
MEDICAL MANAGEMENT
NURSING MANAGEMENT
SUMMARY
Section V: Management of Patients with Long-Term Conditions
26 Management of Patients with Common Movement Disorders
PARKINSON’S DISEASE
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
PARKINSON PLUS DISORDERS
DYSTONIA
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
HUNTINGTON’S DISEASE (HD)
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS
CLINICAL VARIANTS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
SUMMARY
FURTHER INFORMATION
27 Management of Patients with Motor Neurone Disease
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
EVIDENCE-BASED NURSING MANAGEMENT
PSYCHOSOCIAL ISSUES
PALLIATIVE AND END OF LIFE CARE
EXPERIMENTAL TREATMENTS/ CLINICAL TRIALS
SUMMARY
USEFUL CONTACTS
28 Management of Patients with Multiple Sclerosis
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
CLASSIFICATION/TYPES OF MS
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
STAGES OF MS
MEDICAL MANAGEMENT
NURSING MANAGEMENT IN THE DIAGNOSTIC PHASE
NURSING MANAGEMENT IN RELAPSE AND ACUTE EPISODE PHASE
NURSING MANAGEMENT IN PROGRESSIVE PHASE
NURSING MANAGEMENT FOR PEOPLE WITH ADVANCED MS
ROLE OF THE MS SPECIALIST NURSE (MSSN)
SUMMARY
29 Management of Patients with Dementias
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
CLINICAL SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
SUMMARY
FURTHER INFORMATION
30 Management of Patients with Epilepsy
INTRODUCTION
INCIDENCE
AETIOLOGY
PATHOPHYSIOLOGY
SEIZURE CLASSIFICATION
CLASSIFICATION OF EPILEPSIES
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT OF SEIZURES
SEIZURE MANAGEMENT IN THE HOME
INFORMATION PROVISION
REDUCING SEIZURE OCCURRENCE
SUMMARY
31 Management of Patients with Myasthenia Gravis
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
OTHER MYASTHENIC SYNDROMES
CLINICAL FEATURES OF MYASTHENIA GRAVIS
DIAGNOSIS
MEDICAL MANAGEMENT
MYASTHENIC CRISIS
CHOLINERGIC CRISIS
NURSING MANAGEMENT
PSYCHOSOCIAL ISSUES
PROGNOSIS
EMERGING TREATMENTS AND CLINICAL TRIALS
SUMMARY
ACKNOWLEDGEMENTS
Section VI: Management of Patients Following Head and Spinal Trauma
32 Management of Patients with Traumatic Brain Injury
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
CLASSIFICATION
OVERVIEW OF PRIMARY AND SECONDARY INJURY
PATHOPHYSIOLOGY
DIAGNOSIS
ASSESSMENT AND MANAGEMENT
NEURO-REHABILITATION: ACUTE PHASE
NEURO-REHABILITATION: ONGOING PHYSICAL PROBLEMS
PROGNOSIS
THE FUTURE
SUMMARY
33 Management of Patients with Spinal Injury
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
MECHANISMS OF INJURY
PATHOPHYSIOLOGY
PRIORITISING MEDICAL INTERVENTIONS
NURSING MANAGEMENT OF THE ACUTE SCI PATIENT
NURSING ROLE AND RESPONSIBILITIES WITHIN SCI REHABILITATION PROGRAMMES
FUTURE RESEARCH
SUMMARY
USEFUL WEBSITES
Section VII: Management of Patients with Neuropathies and Spinal Disorders and Disease
34 Management of Patients with Disorders of the Vertebral Column and Spinal Cord
INTRODUCTION
AETIOLOGY AND PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS
DIAGNOSIS
INVESTIGATIONS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
COMPLICATIONS FOLLOWING SPINAL SURGERY
POST-OPERATIVE NURSING MANAGEMENT
GENERAL NURSING MEASURES
REHABILITATION
SPECIAL CONSIDERATIONS IN NURSING PATIENTS WITH MALIGNANT SPINAL CORD COMPRESSION (MSCC)
SUMMARY
35 Management of Patients with Guillain–Barré Syndrome and Other Peripheral Neuropathies
INTRODUCTION
EPIDEMIOLOGY
AETIOLOGY
PATHOPHYSIOLOGY
SUB-TYPES OF GUILLAIN–BARRÉ SYNDROME
SIGNS AND SYMPTOMS
DIAGNOSIS
MEDICAL MANAGEMENT
NURSING MANAGEMENT
NURSING MANAGEMENT IN THE ACUTE PHASE
REHABILITATION
SUMMARY
Section VIII: Fundamental Concepts of Neuroscience Nursing
36 Ethical and Legal Issues
INTRODUCTION
ETHICS
LAW
LAW AND ETHICS IN NURSING
CONSENT AND MENTAL CAPACITY
HUMAN RIGHTS
RESOURCE ALLOCATION
RISK MANAGEMENT
END OF LIFE CARE
SUMMARY
37 The History and Development of Neuroscience Nursing
THE BACKGROUND TO A DEVELOPING SPECIALISM
BIRTH OF A SPECIALISM
EPILEPSY
THE NEED FOR EDUCATION
A CONTINUALLY DEVELOPING SPECIALISM
SUMMARY
Index
Neuroscience Nursing
Evidence-Based Practice
This edition first published 2011
© 2011 Blackwell Publishing Ltd
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Library of Congress Cataloging-in-Publication Data
Neuroscience nursing : evidence-based practice / edited by Sue Woodward and Ann-Marie Mestecky.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4051-6356-9 (pbk. : alk. paper) ISBN 978-1-4443-2918-6 (ebk) 1. Neurological nursing. 2. Evidence-based nursing. I. Woodward, Sue (Susan Janet), 1965- II. Mestecky, Ann-Marie.
[DNLM: 1. Nervous System Diseases–nursing. 2. Evidence-Based Nursing. WY 160.5]
RC350.5.N4885 2011
616.8′04231–dc22
2010031661
A catalogue record for this book is available from the British Library.
Contributor List
Thom Aird
Principal Lecturer, Faculty of Health of Health and Social Care, London South Bank University
Kirsty Andrews
Senior Lecturer, Faculty of Health of Health and Social Care, London South Bank University
David Ash
Urology Nurse practitioner & Research Nurse, Princess Royal Spinal Injuries Centre, Northern General Hospital, Sheffield
Beverley Bennett
Senior Lecturer, Faculty of Health & Wellbeing, Sheffield Hallam University
Iain Bowie
Lecturer, Florence Nightingale School of Nursing and Midwifery, King’s College London (Retired)
Mary Braine
Lecturer, School of Nursing, Faculty of Health and Social Care, University of Salford
Chris Brunker
Clinical Nurse Specialist, Neuro ICU St.George’s Healthcare NHS Trust, London
Kathryn Chappell
Highly Specialist Speech and Language Therapist, Surrey Community Health (East Locality), East Surrey Hospital
Maureen Coggrave
Clinical Nurse Specialist, The National Spinal Injuries Centre, Stoke Mandeville Hospital
Neal Cook
Lecturer in Nursing, School of Nursing, University of Ulster
Jane Dundas
Stroke Co-ordinator, Croydon Community Health Services
Ava Easton
Development Manager, The Encephalitis Society, Malton, North Yorkshire
Chris Eberhardie
Honorary Prinicipal Lecturer in Nursing, Faculty of Health and Social Care Sciences, Kingston University and St George’s, University of London
Nikki Embrey
Clinical Nurse Specialist (MS), North Midland MS Service
Karen Harrison Dening
Consultant Admiral Nurse, Barnet Enfield and Haringey Mental Health NHS Trust
Paul Harrison
Clinical Development Officer, Princess Royal Spinal Injuries Centre, Northern General Hospital, Sheffield
Stuart Hibbins
Senior Lecturer, Faculty of Health and Social Care, London South Bank University
Alison Hobden
Lecturer, Department of Health Science, University of Liverpool
Saiju Jacob
Honorary Consultant Neurologist, Queen Elizabeth Neurosciences Centre, University Hospitals of Birmingham NHS Foundation Trust
Leann Johnson
Specialist Registrar, Infectious Diseases Research Dept., North Manchester General Hospital
Katy Judd
Consultant Nurse, Dementia Research Centre, National Hospital for Neurology and Neurosurgery, London
Ehsan Khan
Lecturer, Florence Nightingale School of Nursing and Midwifery, King’s College London
Stephen Leyshon
Primary Care Lead, National Patient Safety Agency, UK
Anthony Linklater
Epilepsy Specialist Nurse, National Hospital for Neurology Neurosurgery, Queen Square London
Vicki Matthews
MS Specialist Nurse Advisor, MS Trust
Pauline McDonald
Parkinson’s Disease Nurse Specialist, Imperial College Heathcare NHS Trust
Anne McLeod
Senior Lecturer in Critical Care, School of Community and Health Sciences, City University, London
Siobhan McLernon
Senior Lecturer, Faculty of Health and Social Care, London South Bank University
Ann-Marie Mestecky
Lecturer, Florence Nightingale School of Nursing and Midwifery, King’s College London
Mary O’Brien
Senior Lecturer, Evidence-Based Practice Research Centre, Faculty of Health, Edge Hill University
Glynis Pellatt
Senior Lecturer, Faculty of Heath and Social Science, University of Bedfordshire
Stephen Pewter
School of Psychology, University of Exeter
Anne Preece
Professional Development Nurse, Neuroscience Critical Care Unit, University Hospitals Birmingham NHS Foundation Trust
Liz Scott
Parkinson’s Disease Nurse Specialist, Buckinghamshire Hospitals NHS Trust
Julia Slark
Clinical Nurse Specialist Stroke, Imperial College Healthcare NHS Trust
Rachel Taylor
Nurse Consultant, Dept of Neurogenetics, The National Hospital for Neurology and Neurosurgery, London
Emma Townsley
Macmillan CNS Neuro-oncology The National Hospital for Neurology and Neurosurgery, UCLH
Colm Treacy
Lecturer, School of Community and Health Sciences, City University, London
Cath Waterhouse
Clinical Nurse Educator, Neuroscience Unit, Royal Hallamshire Hospital, Sheffield
Ian Weatherhead
Lead Nurse, Admiral Nursing Direct For Dementia
Mandy Wells
Consultant Nurse/Head of Dept, Bladder, Bowel and Pelvic Floor Dysfunction, NHS Devon
Ed Wilkins
Consultant and Clinical Director of Infectious Diseases, North Manchester General Hospital
Huw Williams
School of Psychology, Washington Singer Labs, University of Exeter
Sue Woodward
Lecturer, Florence Nightingale School of Nursing and Midwifery, King’s College London
Deborah Yarde
Senior Specialist Nurse Bladder and Bowel Care, NHS Devon
Preface
This is the first evidence-based UK neuroscience nursing textbook for nurses working with people with neurological problems in a wide variety of settings including prevention, primary care, acute and critical care settings, rehabilitation and palliative care. It aims to inform the practice of neuroscience nursing through the report of current research, best available evidence, policy and education and reflects both the richness and the diversity of contemporary neuroscience nursing.
Authors of this edited text have been drawn from nurse specialists, nurse consultants, academics and subject experts from throughout the UK. Each chapter provides a critique of the available evidence underpinning practice, including reference to evidence-based guidelines where relevant. Throughout the text guidelines that have been developed by the National Institute for Health and Clinical Excellence have been referred to in the main. Nurses working in the NHS in Scotland should be mindful that they should also refer to Scottish Intercollegiate Guidelines Network (SIGN) guidelines where these exist.
The text is divided into several different sections covering anatomy and physiology, aspects of assessment, management of patients with a variety of common neurological conditions and other concepts that underpin neuroscience nursing practice. Uniquely, this text includes patients’ perspectives of living with a variety of neurological conditions.
This book is aimed primarily at qualified nurses working specifically with people with neurological problems and has been written in an accessible style appropriate to a staff nurse audience. However, it also provides sufficient detail for more experienced practitioners as the core text underpinning practice and will also enable nursing students who have a particular interest in this field to develop a greater understanding of the specialist management of patients with neurological problems. It also furnishes practitioners in non-specialist areas with the specialist knowledge to enable them to meet the requirements for the National Service Framework for Long-term conditions. Many general, primary care and critical care nurses encounter patients with neurological problems as part of their everyday practice and yet very often they do not have the knowledge and skills to meet these patients’ neurological needs. This book therefore also provides a key reference for non-specialist nurses faced with this situation.
Acknowledgements
We would like to express our thanks to all those who have contributed to the writing and production of this text. It has been a major undertaking and would not have been possible without the expert knowledge of the many contributors. They helped to bring our vision into being.
We would also like to thank the following, who generously gave of their time and expertise in undertaking peer review of the text: Maryanne Ampong, Aimee Aubeeluck, Gill Blackler, Emma Briggs, Chris Brunker, Shuna Colville, Bridgit Dimond, Maria Fitzpatrick, Alison Gallagher, Daiga Heisters, Victoria Hurwitz, Ehsan Khan, Louise Jarrett, Rachael Macarthur, Lindy May, Shanne McNamara, Jacky Powell, Cathy Queally, Tina Stephens, Ben Sullivan, Richard Warner and John Whitaker.
Furthermore we would like to thank all those who shared their experiences of living with a neurological condition or who have experienced injury to the CNS, Alison Wertheimer and Sarah Hill, Ben Edward and the Association for Spina Bifida and Hydrocephalus, amongst others. Their words will help nurses to understand the personal impact of living with a neurological condition. We are also grateful to all those patients and colleagues who agreed to be photographed for this edition.
We thank Sue Scullard for her time in designing a number of the figures.
Sue would like to thank her husband and children for their support and patience.
Ann-Marie would like to thank David, for his good humour, patience, support and above all encouragement, as well as Joseph, Mum and Dad.
Section I: Anatomy and Physiology of the Nervous System
1
Cells of the CNS and How They Communicate
Colm Treacy
INTRODUCTION
The neurone (or nerve cell) is the most important component of the nervous system. Its main function is to rapidly process and transmit information. The human nervous system contains about 300–500 billion neurones (approximately 80,000/mm2), integrated into an intricate functional network by millions of connections with other neurones. Neurones communicate primarily via chemical synapses. The action potential is the fundamental process underlying synaptic transmission. It occurs as a result of waves of voltage that are generated by the electrically excitable membrane of the neurone.
This chapter will explore the histology of the nervous tissue and the physiology of neurotransmission.
COMPONENTS OF THE NEURONE AND THEIR FUNCTIONS
Neurones contain components and organelles that are crucial to normal cellular function and these generally resemble those of non-neuronal cells. Neurones of various types have different morphologies and functional features, depending on their location in the central nervous system (CNS). The prototypical neurone (Figure 1.1) consists of a stellate cell body (soma), a single axon that emerges from the soma, a number of thin processes called dendrites (the axon and dendrites are collectively known as neurites) and points of functional contact at the axon terminal with other cells, glands or organs, called synapses. The integrative functions of these unique structures are what differentiate neurones from non-neuronal cells and underlie the generation and transmission of information, which is so unique and fundamental to nervous system activity.
Figure 1.1 Diagram of a multipolar neurone. Note that the processes of other neurones make synaptic contacts with it. Synapses may be formed, as illustrated, with the soma or with the dendrites, although other types of synapses also occur.
Reproduced from Maria A Patestas and Leslie P Gartner, A Textbook of Neuroanatomy, Wiley-Blackwell, with permission.
Like other cells in the body, the neurone is enclosed by a bi-layered lipoprotein-rich cell membrane, called the neuronal membrane. This membrane is approximately 5–7.5 nm thick and separates the cytoplasmic contents from the extracellular environment.
As in non-neuronal cells, the soma, (or cell body, also known as the perikaryon), is roughly spherical in shape and measures around 20 µm in diameter. The soma of smaller neurones may measure as little as 5 µm, whereas in the case of large motor neurones, they can be as much as 135 µm in diameter. The soma is the site of routine cellular housekeeping functions, including the synthesis of all the neuronal proteins that are necessary for the upkeep of the axon and axon terminals (Longstaff, 2000). In common with non-neuronal cells, the soma also includes important cellular organelles, such as the nucleus, Golgi apparatus, endoplasmic reticulum (ER), ribosomes, lysosomes and mitochondria.
The nucleus
The nucleus is approximately 5–10 µm in diameter and is surrounded by a granular, double-layered membrane, known as the nuclear envelope, which is perforated by small pores measuring around 0.1 µm wide. These small pores act as passageways between the nucleoplasm (interior of the nucleus) and the surrounding cytoplasm. By comparison with non-neuronal cells, the nuclei of neurones tend to be larger, which is thought to be related to the high levels of protein synthesis within the neurone. The nucleus contains the genetic material, deoxyribonucleic acid (DNA), which is responsible for directing the metabolic activities of the cell. Messenger ribonucleic acid (mRNA) is also found within the nucleus. It is responsible for copying the specific genetic instructions from the DNA (transcription) for protein synthesis and carrying it to the site of protein production in the cytoplasm.
The rough endoplasmic reticulum (RER)
The RER is adjacent to the nucleus and is composed of rows of plate-like membranous sacs, which are covered in granular ribosomes. The RER synthesises the majority of protein needed to meet the functional demands of the neurone. It does this under the direction of mRNA. The ribosomes build proteins from amino acids delivered by transfer RNA from the genetic instructions held within messenger RNA. Rough ER is especially abundant in neurones, more so than in glia or other non-neuronal cells. It is densely packed within the soma and the shafts of dendrites, giving rise to distinct structures called Nissl bodies.
The smooth endoplasmic reticulum (SER)
The SER is made up of an extensive network of stacked membranous structures that are continuous with the nuclear membrane and RER. It is thought to be the main site of protein-folding. Smooth ER is heterogeneous in function and, depending on its location in the soma, it has important functions in several metabolic processes including protein synthesis, carbohydrate metabolism and regulation of calcium, hormones and lipids. It also serves as a temporary storage area for vesicles that transport proteins to various destinations throughout the neurone.
The Golgi apparatus
The Golgi apparatus is a highly specialised form of smooth endoplasmic reticulum that lies furthest away from the nucleus. In most neurones, the Golgi apparatus completely surrounds the nucleus and extends into the dendrites; however it does not extend into axons. It is composed of aggregated, smooth-surfaced cisternae that are perforated by circular openings to allow the two-way passage of proteins and other molecules. It is surrounded by a mixed group of smaller organelles, which includes mitochondria, lysosomes, multivesicular bodies and vacuoles. The primary function of the Golgi apparatus is to process and package large molecules, primarily proteins and lipids, that are destined for different parts of the neurone such as the axon or dendrites.
Lysosomes
Lysosomes are the principal organelles responsible for the degradation of cellular waste-products. They are membrane-bound vesicles that contain various enzymes (acid hydrolases) that catalyse the breakdown of large unwanted molecules (bacteria, toxins, etc.) within the neurone. Lysosomes are more numerous and conspicuous in injured or diseased neurones. For this reason, they are often used as biomarkers for ageing and neurodegeneration. Multivesicular bodies are derived from primary lysosomes and are made up of several tiny spherical vesicles that also contain acid hydrolases. They are small oval shaped, single membrane-bound sacs, approximately 0.5 µm in diameter and have also been noted in various forms of neurodegeneration.
Mitochondria
Mitochondria are the ‘power houses’ of cells. They are responsible for oxidative phosphorylation and cellular respiration – crucial for the function of all aerobic cells, including neurones. Measuring between 1 µm and 10 µm in length, these organelles are concentrated in the soma and the synaptic terminals, where they produce adenosine triphosphate (ATP), the cell’s energy source (Hollenbeck and Saxton, 2005). In addition to energy production, mitochondria also perform a number of other essential functions within the neurone, which include buffering cytosolic calcium levels (Gunter et al., 2004) and sequestering proteins involved in apoptosis (see Chapter 32) (Gulbins et al., 2003). The complex folding of the cristae within mitochondria provides a large surface area to harbour a number of enzymes. These enzymes, which diffuse through the mitochondrial matrix, catalyse the critical metabolic steps involved in cellular respiration. Because of the high energy demands of cellular function and protein synthesis, the number of mitochondria correlates with the neurone’s level of metabolic activity.
The cytoskeleton
The cytoskeleton provides a dynamically regulated ‘scaffolding’ that gives neurones their characteristic shape and facilitates the transport of newly synthesised proteins and organelles from one part of the neurone to another (Brown, 2001). The main components of the cytoskeleton include microfilaments, microtubules and neurofilaments.
Microfilaments
Microfilaments are particularly abundant in axons and dendrites (neurites), but they are also distributed throughout the neuronal cytoplasm. They are also abundant in the expanded tips of growing neurites, known as growth cones (Dent et al., 2003; Kiernan, 2004). They are made from a polymer called actin, a contractile protein that is most commonly associated with muscle contraction. They are composed of two intertwined chains of actin, arranged to create double helix filaments, measuring around 4–6 nm in diameter and a few hundred nanometres in length. The main role of microfilaments is the movement of cytoskeletal and membrane proteins.
Microtubules
Microtubules measure 20–24 nm in diameter and can be several hundred nanometres in length. They are made of strands of globular protein, tubulin, arranged in a helix around a hollow core, to give the microtubule its characteristic thick-walled, tube-like appearance. Microtubules play an important role in maintaining neuronal structure and they also act as tracks for the two-way transport (see: Axonal transport ) of cellular organelles.
Neurofilaments (NFs)
Neurofilaments are a type of intermediate filament (IF), seen almost exclusively in neuronal cells. Measuring about 10 nm in diameter, neurofilaments can be several micrometres long and they frequently occur in bundles (Raine, 1999). Like their IF counterparts in non-neuronal cells, they are assembled in a complex series of steps that give rise to solid, rod-like filaments. These filaments are made up of polypeptides that are coiled in a tight, spring-like configuration. They are sparsely distributed in dendrites but they are abundant in large axons, where they facilitate axonal movement and growth.
Axonal transport
Protein synthesis does not usually occur within the axon, therefore any protein requirements for the repair and upkeep of the neurone must be met by the soma. In the soma, various components (including organelles, lipids and proteins) are assembled and packaged into membranous vesicles and transported to their final cellular destination by a process known as axonal transport (axoplasmic transport). Axonal transport involves movement from the soma, towards the synapse, called anterograde transport and movement away from the axon, towards the soma, called retrograde transport.
Axonal transport can be further divided into fast and slow subtypes. Fast anterograde transport occurs at a rate of 100–400 mm/day and involves the movement of free elements including synaptic vesicles, neurotransmitters, mitochondria, and lipid and protein molecules (including receptor proteins) for insertion/repair of the plasma membrane. Slow anterograde transport on the other hand, occurs at a rate of 0.3–1 mm/day and involves the movement of soluble proteins (involved in neurotransmitter release at the synapse) and cytoskeletal elements (Snell, 2006). Both types of anterograde transport are mediated by a group of motor proteins called kinesins (Brown, 2001). Retrograde transport involves the movement of damaged membranes and organelles towards the soma, where they are eventually degraded by lysosomes (found only in the soma). It is mediated by a different kind of motor protein known as dynein.
The axon
The organelles and cellular components already discussed are not unique to neurones and may be found (with a few exceptions) in almost any cell in the body. However, the main feature that distinguishes neurones from other cells is the axon, the projection that emerges from the soma, and its associated elaborate process of dendrites. Under the microscope, it is hard to distinguish the axon from dendrites of some neurones, but in others it is easily identified on the basis of length. Whilst some neurones have no axons at all (e.g. the amacrine cell, found in the retina), most neurones have a single axon. The axons of some neurones branch to form axon collaterals, along which the impulse splits and travels to signal several cells simultaneously.
Neurones can be broadly classified according to length of their axonal processes. Golgi type I neurones contain long-projecting axonal processes, whilst Golgi type II neurones have shorter axonal processes. Another way of classifying neurones is according to their location within the central nervous system, or on the basis of their morphological appearance. Examples of specific types of neurones include Basket, Betz, Medium spiny, Purkinje, Renshaw and Pyramidal cells. Neurones may also be classified according to the number of branches that originate from the soma (Figure 1.2):
Unipolar or pseudounipolar neurones are characterised by a single neurite that emerges and branches or divides a short distance from the soma. Most sensory neurones of the peripheral nervous system are unipolar.Bipolar neurones are characterised by a single axon and a single dendrite that emerge from opposite ends of an elongated soma. These types of neurones are found in the sensory ganglia of the cochlear and vestibular system and also in the retina.Multipolar neurones are characterised by a number of dendrites that arise and branch close to the soma. They make up the majority of neurones in the CNS.Figure 1.2 Structural classification of neurones. Breaks indicate that axons are longer than shown. (a) Multipolar neurone. (b) Bipolar neurone. (c) Unipolar neurone.
Reproduced from Principles of Anatomy and Physiology 12e by Gerard Tortora and Bryan Derrickson. Copyright (2009, John Wiley & Sons). Reprinted with permission of John Wiley & Sons Inc.
The primary function of the axon is to transmit electrochemical signals to other neurones (sometimes over a considerable distance). Transmission occurs at rates that are appropriate to the type and function of the individual neurone. Because of this, the axonal length of a given neurone may vary from as little as a few micrometres, to over 1 metre in humans. For example, the sciatic nerve, which runs from the base of the spine to the foot, may extend a metre or even longer. Typical diameters can range from 0.2 to 20 µm for large myelinated axons.
The axon has four regions: the axon hillock (or trigger zone), the initial segment, the axon proper and the axon terminals. The axon hillock originates at the soma; adjacent to the axon hillock is the initial segment. The plasma membranes of these two regions contain large numbers of specialised, voltage sensitive ion channels and most action potentials originate in this area (see below: Action potentials). Beyond the initial segment, the axon proper maintains a relatively uniform, cylindrical shape, with little or no tapering. The consistent diameter of the axon (axon calibre) is maintained by components of the cytoskeleton and this feature also helps to maintain a uniform rate of conduction along the axon. In addition to the axon calibre, the rate of conduction along the axon is influenced by the presence of the myelin sheath, which begins near the axon hillock and ends short of the axon terminals.
Myelination
Myelin is a specialised protein, formed of closely apposed glial cells that wrap themselves several times around the axon (Kiernan, 2004). In the central nervous system, the glial cells making up the myelin sheath are called oligodendrocytes, whereas in the peripheral nervous system, they are known as Schwann cells (see: Neuroglia). Several axons may be surrounded simultaneously by a single glial cell.
The myelin sheath insulates the axon and prevents the passive movement of ions between the axoplasm and the extracellular compartment. Myelinated axons also contain gaps at evenly-spaced intervals along the axon, known as nodes of Ranvier (Figures 1.1 and 1.3). These nodes are the only points where the axonal membrane is in direct contact with the extracellular compartment and where ions can readily flow across the axonal membrane. Therefore, any electrical activity in the axon is confined to this part. In myelinated axons, the nodes of Ranvier contain clusters of voltage-gated sodium (Na+) channels, whereas in unmyelinated axons, these voltage-gated Na+ channels are distributed uniformly along the whole of the axon. This feature enables the axon to conduct action potentials over long distances, with high fidelity and a constant speed, and underlies the ability of the neurone to conduct impulses by a process known as saltatory conduction. Saltatory conduction (from the Latin saltare, to ‘jump’), enables action potentials to literally jump from one node to the next, rather than travelling along the membrane (Ritchie, 1984). Saltation allows significantly faster conduction (between 10 and 100 metres per second) in myelinated axons, compared with the slower conduction rates seen in their unmyelinated counterparts.
Figure 1.3 A single oligodendrocyte is capable of myelinating a single internode of numerous axons.
Reproduced from Maria A Patestas and Leslie P Gartner, A Textbook of Neuroanatomy, Wiley-Blackwell, with permission.
The increased speed afforded by saltatory conduction therefore allows the organism to process information more quickly and to react faster, which confers a distinct advantage for survival. In addition to this, the high concentrations of ion channels at the nodal intervals conserve energy, as they reduce the requirements for sodium–potassium pumps throughout the axonal membrane. Multiple sclerosis (MS) is a demyelinating disease, characterised by patchy loss of myelin in the brain and spinal cord. As a result of the demyelinating process, plaques develop in the white matter, which result in a reduced concentration of sodium ion channels at the nodes of Ranvier and a slowing of action potentials (see Chapter 28).
The terminal portion of the axon is known as the axon terminal, where the axon arborises (or branches) and enlarges. This region goes by a variety of other names, including the terminal bouton, the synaptic knob or the axon foot. The axon terminal contains synaptic vesicles which contain neurotransmitters (see: Neurotransmitters).
Dendrites
Dendrites are the afferent components of neurones, i.e. they receive incoming information. The dendrites (together with the soma) provide the major site for synaptic contact made by the axon endings of other neurones. Dendrites are generally arranged around the soma of the neurone in a stellate (or star-shaped), configuration. In some neurones, dendrites arise from a single trunk, from which they branch out, giving rise to the notion of a dendritic tree (Raine, 1999). Under the microscope, it can be difficult to distinguish the terminal segments of axons from small dendrites, or small unmyelinated axons. However, unlike the diameters of axons, the main distinguishing feature of dendrites is that they taper, so that successive branches become narrower as they move further away from the soma. In addition, unlike axons, small branches of dendrites tend to lack any neurofilaments, although they may contain fragments of Nissl substance; however, large branches of dendrites proximal to the axon may contain small bundles of neurofilaments. The synaptic points of contact on dendrites occur either along the main stems or at small eminences known as dendritic spines – the axon terminals of other neurones adjoin these structures.
NEUROGLIA
Neuroglia (Figure 1.4), usually referred to simply as glia (from the Greek word meaning ‘glue’) or glial cells, are morphologically and functionally distinct from neurones. Neuroglia comprise almost half the total volume of the brain and spinal cord. They are smaller than neurones and more numerous – outnumbering them almost 10-fold (Snell, 2006). Although they have complex processes extending from their cell bodies, they lack any axons or dendritic processes.
Figure 1.4 Neuroglia of the central nervous system (CNS).
Reproduced from Principles of Anatomy and Physiology 12e by Gerard Tortora and Bryan Derrickson. Copyright (2009, John Wiley & Sons). Reprinted with permission of John Wiley & Sons Inc.
Previously it was assumed that glia do not participate directly in any signalling or synaptic interactions with other neurones. However, recent studies have indicated that their supportive functions help to define synaptic contacts and that they are crucial facilitators of action potentials. Other roles attributed to neuroglia include: maintaining the ionic environment in the brain, modulating the rate of signal propagation, and having a synaptic action by controlling the uptake of neurotransmitters. They also provide a scaffold for some aspects of neural development, and play an important role in recovery from neuronal injury (or, in some instances, prevention). They also have an important nutritive role and release factors which modulate pre-synaptic function.
There are four main types of glial cells in the mature CNS: astrocytes, oligodendrocytes, microglial cells and ependymal cells – the description, location and function of these are summarised in Table 1.1.
Table 1.1 Description, location and function of specific neuroglia.
CNS – central nervous system; PNS – peripheral nervous system; BBB – blood–brain barrier; CSF – cerebrospinal fluid.
COMMUNICATION BY NEURONES
The resting membrane potential
The neuronal membrane is about 8 nm thick and is made up of a hydrophobic lipid bi-layer, which acts as a selective barrier to the diffusion of ions between the cytoplasm (intracellular) and extracellular compartments. The unequal distribution of ions (positively or negatively charged atoms) either side of the cell membrane results in a difference of electrical charge (potential difference) between the inside and the outside of the cell membrane. The overall effect of this gives rise to the resting membrane potential. It is called the resting membrane potential because it occurs when the neurone is in an unstimulated state, i.e. not conducting an impulse. In this state, the neurone is said to be polarised, because there is a relative excess of positive electrical charge outside the cell membrane and a relative excess of negative charge inside. To maintain a steady resting membrane potential, the separation of charges across the membrane must be constant, so that any efflux of charge is balanced against any charge influx (Gilman and Winans Newman, 2003). By convention therefore, the charge outside the neuronal membrane is arbitrarily defined as zero, whilst the inside of the neurone (relative to the outside) is negatively charged (−70 mV).
The extracellular fluid contains a dilute solution of sodium (Na+) and chloride (Cl−) ions. By contrast, the axoplasm contains high concentrations of potassium (K+) ions and organic anions (large negatively charged organic acids, sulphates, amino acids and proteins) (Holmes, 1993). Two passive forces (diffusional and electrostatic) act simultaneously upon these ions to maintain the resting potential. Diffusional (chemical) forces drive Na+ ions inwards and K+ ions outwards, from areas of high concentration to areas of low concentration, i.e. down their respective chemical concentration gradients. Secondly, electrostatic forces (charge) move ions across the membrane, in a direction that depends on their electrical charge, so that the positively charged Na+ and K+ ions are attracted towards the negatively-charged cell interior (Waxman, 2000).
In addition to these diffusional and electrostatic forces, the resting potential is also influenced by the action of ion-specific membrane-spanning channels. These ion channels selectively allow the passage of certain ions, whilst excluding others. Two types of ion channels exist, which can be in an open or closed state: voltage gated and non-gated ion channels. Non-gated channels, which are primarily important in maintaining the resting potential are always open and are not influenced significantly by extrinsic factors, these gates allow for the passive diffusion of K+ and Na+ ions. Gated channels, however, open and close in response to specific electrical, mechanical, or chemical signals and their conformational states (i.e. whether they are open or not) depend on the voltage across them (Longstaff, 2000). When the neurone is polarised (i.e. is at resting membrane potential) these gates are closed.
At resting membrane potential, the neuronal membrane is relatively permeable to K+ ions, which passively diffuse out of the cell, through non-gated potassium channels. This causes a net increase in the negative charge on the inside of the cell membrane. In addition to the outward leakage of potassium, negatively charged anions (which cannot diffuse across the membrane because of their large size) add further to the overall negative intracellular charge. The majority of sodium channels are closed at resting membrane potential, so diffusion of Na+ along its own ionic gradient is prevented. In addition, the sodium–potassium pump actively transports Na+ ions out of the cell, while taking in K+. The pump moves three sodium ions out of the cell for every two potassium ions that it brings in. The sodium–potassium pump therefore moves Na+ and K+against their net electrochemical gradients, which requires the use of energy (from the hydrolysis of ATP).
As long as the force of the K+ ions diffusing outwards exceeds the oppositely oriented electrical charge, a net efflux of K+ continues from inside the cell. But as more K+ ions travel out (along the K+ concentration gradient), the electrical force (negative charge) attracting K+ ions into the cell, gradually increases (Wright, 2004; Barnett and Larkman, 2007). If a state was reached whereby the chemical and electrical forces balanced, (equilibrium potential of potassium) there would be no K+ ion movement. This equilibrium potential for potassium occurs at −90 mV. However an equilibrium potential for potassium is never quite reached due to the small continual leakage of sodium from the cell.
Changes in the resting membrane potential
Changes in the resting membrane potential will occur when a stimulus causes gated ion channels to open thereby changing the membrane’s permeability to an ion. Depending on the type and strength of the stimulus, the change in the resting membrane potential will produce either a graded potential or an action potential. If the stimulus alters a local area of the membrane only and does not conduct far beyond the point of stimulation it is referred to as a graded potential (see below: Neurotransmitters). If the stimulus is of sufficient strength to cause a change in the entire membrane potential the response is referred to as an action potential.
An increase in the negativity of the resting membrane potential, e.g. −70 mV to −80 mV is referred to as hyperpolarisation. Conversely, any reduction in the negativity of the membrane potential, e.g. −70 mV to −65 mV, is referred to as depolarisation.
The action potential
An action potential (Figure 1.5) is initiated when a stimulus causes the voltage gated sodium channels to open. Sodium ions rapidly diffuse through the neuronal membrane down their electrochemical gradient attracted by the negative charge inside the neurone. The most common site of initiation of the action potential is the axon hillock (also called the trigger zone), where the highest concentration of voltage-gated ion channels is found (previously described).
Figure 1.5 Action potential in a neurone.
The rush of Na+ into the neurone briefly reverses the polarity of the membrane from a negative charge of −70 mV (resting membrane potential) typically to a positive charge of +30 mV (depolarisation). The influx of Na+ and subsequent depolarisation of one section of the axonal membrane, i.e. the trigger zone, is the stimulus to open additional voltage gated sodium channels in the adjacent membrane, thus the depolarisation spreads forward along the axonal membrane. The voltage gated sodium channels are open only briefly, they become inactivated when the charge reaches +30 mV, stopping any further influx of Na+ into the neurone. This brief alteration in charge lasts approximately 5 milliseconds.
Whilst the voltage gated sodium channels are closing, voltage-gated potassium channels open resulting in a huge efflux of K+ ions (downward stroke) which continues until the cell has repolarised to its resting potential (from +30 mV to −70 mV). During repolarisation the voltage gated sodium channels remain inactivated.
Following repolarisation, the neurone is briefly unyielding to any further action potentials, a phase known as the recovery/relative refractory period. The absolute refractory period is the time during which a second action potential absolutely cannot be initiated (see Figure 1.5). The sodium–potassium pump actively transports K+ and Na+ ions across the membrane, (against their respective chemical concentration gradients), to re-establish the resting potential.
Threshold stimulus and the all-or-none phenomenon
The stimulus must depolarise the membrane potential to a threshold value, which is typically to −55 mV for an action potential to occur. If the membrane does not reach the threshold value an action potential will not occur. If the threshold is reached the action potential will propagate forward at maximal strength regardless of the strength of the initial stimulus. Therefore the action potential will occur maximally or not at all. This is the ‘all-or-none phenomenon’.
NEUROTRANSMISSION
Synapses
Once the action potential reaches the axon terminal it needs to transfer to another cell. The synapse (Figure 1.6) is the location of signal transmission from one neurone to another or, in most cases, many other neurones. The synapse is typically between the axon terminal of a neurone (pre-synaptic) and the surface of a dendrite or cell body of another neurone (post-synaptic). The number of synaptic inputs to a typical neurone in the human nervous system ranges from 1 to about 100,000, with an average in the thousands.
Figure 1.6 An example of an ionotropic effect occurring at a synapse indicating the events that occur before, during, and after the release of neurotransmitter substances.
Reproduced from Maria A Patestas and Leslie P Gartner, A Textbook of Neuroanatomy, Wiley-Blackwell, with permission.
Two types of synapse exist: electrical and chemical. In electrical synapses, ion channels (connections) arrange themselves around a central hollow core to form gap junctions. These gap junctions allow electrical coupling and the passage of water, small molecules (<1.2 nm diameter) and various ions between adjacent cells. Electrical synapses are predominantly associated with electrical activity in cardiac and smooth muscle. They are also found between astrocytes and are crucially involved in the coupling of horizontal cells found in the retina. Electrical signalling is bi-directional in electrical synapses.
In humans, the majority of synapses are chemical synapses and therefore rely on the release of neurotransmitters and their binding with receptor proteins on the post-synaptic membrane of the target neurone. Typically, the pre-synaptic terminal is immediately adjacent to a post-synaptic region but there is no physical continuity between these regions. Instead, the components communicate by chemical neurotransmitters that cross the extracellular space known as the synaptic cleft to bind to receptors in the post-synaptic region.
Neurotransmitters
Neurotransmitters are the molecules responsible for chemical signalling in the nervous system. Neurotransmitters are synthesised in the soma and are transported to the terminal parts of the axon (near the synaptic region), where they are packaged into vesicles and stored in areas known as active zones, ready for release at the synapse. When an action potential reaches the axon terminal voltage gated calcium channels open, the influx of calcium ions cause the vesicles to fuse with the pre-synaptic membrane and vesicular contents are released in discreet packets or quanta, into the synaptic cleft, by a process of exocytosis. Each quantum represents the release of the contents of a single vesicle (around 4000 molecules of neurotransmitter) (Longstaff, 2000). Following exocytosis, the vesicular membrane proteins are recycled by a process known as endocytosis .
The first neurotransmitter to be described was acetylcholine (ACh), by Loewi in 1926, following his extensive work on frog cardiac muscle. Subsequently, a wide range of other neurotransmitters have been described, each of which may be chemically differentiated on the basis their molecular structure, patterns of distribution, localisation to specific brain areas and their association with specific functions (Michael-Titus et al., 2007).
The effects of the main neurotransmitters and their mode of action are summarised in Table 1.2.
Table 1.2 Key central nervous system neurotransmitters.
In addition to the principal neurotransmitters, other chemicals can also modulate the impact of neurotransmitter on the post-synaptic neurone. They do this by enhancing, prolonging, inhibiting or limiting the effect of a particular neurotransmitter on the post-synaptic neurone, so that the response of metabotropic receptors (see below) may last several minutes or longer. These substances are called neuromodulators, because they modulate the response of the neurone to other inputs. It is widely accepted that some molecules can act simultaneously as a neurotransmitter or a neuromodulator (termed co-transmission) and classification largely depends on whether its action occurs over a long range or is localised to the synapse.
Neurotransmitters exert their effects on post-synaptic receptors of target neurones. The action of a given neurotransmitter on a target neurone or indeed peripherally on a particular effector organ (see Chapter 5) largely depends on the types of receptors present on that target. Most types of neurotransmitters have a number of specific receptor subtypes that they can activate. These receptors can be classified according to their overall structure and function. The effects of neurotransmitters depend on the summation of responses at the post-synaptic membrane.
Two broad superfamilies of receptor have been described, which include ionotropic and metabotropic receptors. The ionotropic, or ligand-gated ion channel receptors, are made up of ion-selective channels that are integral to the receptor. Binding of neurotransmitter directly results in the selective opening or closure of the channel and directly increasing or decreasing its permeability to particular ions, as described above.
Ionotropic or ligand-gated ion channel receptors
The binding of a neurotransmitter to an ionotropic receptor will cause a change in the post-synaptic membrane potential by either bringing about the opening or closing of ion channels. When the neurotransmitter causes the opening of positive ion channels (e.g. Na+ channels) in the post-synaptic membrane the net effect is to reduce the negativity of the membrane potential (e.g. from −70 mV to −68 mV). This is known as an excitatory post-synaptic potential (EPSP). This is below the level required to lift the potential to threshold level for an action potential to occur. When the neurotransmitter causes the opening of potassium channels, thereby allowing positive ions to leave the neurone, or opens chloride (Cl−) channels the effect is to reduce the resting potential i.e. make it more negative this is known as inhibitory post-synaptic potential (IPSP). The IPSP reduces the post-synaptic neurone’s ability to generate an action potential. These small shifts are called graded potentials. Whether an action potential is generated or not depends on the summation of the graded potentials. Several EPSPs are needed to convert resting potential to an action potential. Summation may be temporal (the cumulative effect of repeated impulses from a single synapse) or spatial (the net effect of simultaneous impulses from different synapses along the membrane).
The second superfamily of receptors are known as the metabotropic receptors. Binding of neurotransmitters to these receptors has longer lasting effects on the post-synaptic cell. When a neurotransmitter binds to these receptors, small intracellular proteins called G-proteins are activated. G-proteins exert their effects on the post-synaptic membrane by binding ion channels directly, or by indirectly activating second messengers. Second messengers are molecules that are produced or released inside the cell; the most common being cyclic-adenosine monophosphate (cAMP). Second messengers can activate other enzymes in the cytosol that can regulate ion-channel function or alter the metabolic activities of the cell, hence the name metabotropic.
Inactivation and removal of neurotransmitters
Typically, neurotransmitter binding takes less than 5 µs, but not all neurotransmitter that has been released binds to the post-synaptic membrane of the target neurone. The distance between the pre- and post-synaptic membrane is as little as 12 nm across, but due to reuptake of neurotransmitter, passive diffusion away from the synaptic cleft and inactivation by various enzymes, the amount of transmitter available for binding is reduced. For example, enzymatic degradation of ACh (by acetylcholinesterases) takes place in the synaptic cleft at the neuromuscular junction or other cholinergic synapses. These enzymes cleave ACh into its inactive components, acetate and choline, which are recycled and used to synthesise further ACh by combination with acetyl-coenzyme-A.
Other neurotransmitters are inactivated in a similar way, or they may be inactivated by direct removal from the synaptic cleft. Direct removal from the synaptic cleft is carried out by reuptake transporters, which actively transport unused neurotransmitter to surrounding neurones or glia. The importance of the mechanisms of reuptake is highlighted by the impact of certain drugs on brain function. Illicit drugs, such as ecstasy (3, 4-methylenedioxy-N-methamphetamine; MDMA), for example, block the reuptake of serotonin (5-hydroxytryptamine; 5HT). This results in an excess of serotonin in the synaptic cleft, which contributes to its euphoric effects (McCann et al., 2005). Similarly, other illicit drugs such as cocaine inhibit the reuptake of dopamine, which is responsible for its euphoric and addictive effects (Mash et al., 2002). Of course, neurotransmitter reuptake blockade can also have more useful, therapeutic applications, for example in the treatment of depression with selective serotonin reuptake inhibitors (SSRIs), which block the reuptake of serotonin. The therapeutic use of drugs that inhibit reuptake of neurotransmitters will be discussed in the relevant chapters on specific diseases.
SUMMARY
The nervous system is vital for maintaining the homeostasis of the body. It continuously receives information which it must process and rapidly respond to. These vital functions are made possible by the generation of action potentials and chemical synapses. Neurotransmitters released at a synapse can have either excitatory or inhibitory effects whereas neuromodulators prolong, inhibit, or limit the effect of a particular neurotransmitter on the post-synaptic neurone.
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2
The Structural and Biochemical Defences of the CNS
Ehsan Khan
INTRODUCTION
The central nervous system (CNS) is one of the most delicate structures within the body. It is a vital part of the body that needs to function continuously to maintain life. The tissue that comprises the CNS is extremely delicate, and the CNS is consequently extremely susceptible to both mechanical and chemical insult. To reduce the risk of mechano-chemical injury, protection of this delicate system comprises structural as well as biochemical defences. This chapter will describe the defensive features of the CNS, providing the reader with a conceptual and functional understanding of these structures and processes. This information will help the reader to understand the clinical consequences of failure of these structures and processes.
The defences of the central nervous system include the following.
Structural defences:
Bony encasementMembranes – meninges and the blood–brain barrier (BBB)Cerebrospinal fluid (CSF)Biochemical defences:
EnzymesEfflux proteinsMetabolic enzymesBONY ENCASEMENT
The skull
The skull is made up of a number of flat bones that are joined together by serrated junctions known as sutures (Figure 2.1). The skull comprises the cranial and facial bones. The cranial bones include the brain casing or the skull cap (the calvaria) and the bones of the cranial cavity floor. The sinusoidal flat bones of the skull have a spongy diploe centre that is sandwiched between the hard external and internal compact layers of the skull bone. This arrangement affords the skull considerable strength and resistance to trauma while maintaining a low weight. It provides protection together with support and ease of movement of the head.
Figure 2.1 Medial view of sagittal section of skull. Although the hyoid bone is not part of the skull, it is included in the illustration for reference.
Reproduced from Principles of Anatomy and Physiology 12e by Gerard Tortora and Bryan Derrickson. Copyright (2009, John Wiley & Sons). Reprinted with permission of John Wiley & Sons Inc.
The calvaria
The skull cap or calvaria is formed by the frontal bone, two parietal bones and the occipital bone.
The fontal bone
