Tutor Neurological Examination ..Pocket Tutor.. 2nd Edition 2017 PDF
Tutor Neurological Examination ..Pocket Tutor.. 2nd Edition 2017 PDF
Tutor Neurological Examination ..Pocket Tutor.. 2nd Edition 2017 PDF
pocket tutor
Examination
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Neurological
pocket tutor
Examination
John A Goodfellow
Honorary Clinical Academic Fellow
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University of Glasgow
Glasgow, UK
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Editorial Advisor
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Neel Burton BSc MBBS MRCPsych MA (Phil) AKC
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Tutor in Psychiatry
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Green Templeton College
University of Oxford
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Oxford, UK
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© 2012 JP Medical Ltd.
Published by JP Medical Ltd, 83 Victoria Street, London, SW1H 0HW, UK
Tel: +44 (0)20 3170 8910 Fax: +44 (0)20 3008 6180
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Email: [email protected] Web: www.jpmedpub.com
The rights of John Goodfellow to be identified as the author of this work have been asserted
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by him in accordance with the Copyright, Designs and Patents Act 1988.
All rights reserved. No part of this publication may be reproduced, stored or transmitted in
any form or by any means, electronic, mechanical, photocopying, recording or otherwise,
except as permitted by the UK Copyright, Designs and Patents Act 1988, without the prior
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permission in writing of the publishers. Permissions may be sought directly from JP Medical
Ltd at the address printed above.
All brand names and product names used in this book are trade names, service marks,
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trademarks or registered trademarks of their respective owners. The publisher is not
associated with any product or vendor mentioned in this book.
Medical knowledge and practice change constantly. This book is designed to provide
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accurate, authoritative information about the subject matter in question. However, readers
are advised to check the most current information available on procedures included or from
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the manufacturer of each product to be administered, to verify the recommended dose,
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formula, method and duration of administration, adverse effects and contraindications. It
is the responsibility of the practitioner to take all appropriate safety precautions. Neither
the publisher nor the author assumes any liability for any injury and/or damage to persons
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or property arising from or related to use of the material in this book.
This book is sold on the understanding that the publisher is not engaged in providing
professional medical services. If such advice or services are required, the services of a
competent medical professional should be sought.
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ISBN: 978-1-907816-30-7
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Library of Congress Cataloging in Publication Data
A catalog record for this book is available from the Library of Congress
JP Medical Ltd is a subsidiary of Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India.
Publisher: Richard Furn
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Design: Designers Collective Ltd
Indexed, typeset, printed and bound in India.
Foreword
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cal school, and would not have predicted that outcome at the
time. Richard Smith (former editor of the British Medical Journal)
described the neurologist as ‘a brilliant and forgetful man with
a bulging cranium, a loud bow tie, who reads Cicero in Latin
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for pleasure, hums Haydn sonatas, talks with ease about bits
of the brain you’d forgotten existed, adores diagnosis and rare
syndromes, and – most importantly – never bothers about
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treatment.’ I do like making a diagnosis, talking about the brain,
and enjoy quoting eponymous syndromes but the rest has,
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thankfully, never been my experience.
Like most medical students, many GPs and other hospital
specialists when asked later in their careers, I too once suf-
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fered from what has been termed by several commentators as
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‘neurophobia’. Now I feel the excitement of a test pilot when
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approaching the consultation, and it has become one of my
own passions to help dispel this fear and share the knowledge
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needed to ‘fly’ a neurological case.
Accepting there is a core of principles that will allow all cli-
nicians to interpret and localise neurological symptoms is not
dumbing down, but a welcome blast of common sense in an
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increasingly specialised world of medical practice. Neurological
disorders will become more prevalent as populations age, and
a high proportion of acute medicine already has a neurological
flavour. Yet only a tiny proportion of medical school curricula
are dedicated to the teaching of clinical neurology and few
non-neurologists experience any at postgraduate level.
John Goodfellow ‘got it’ as a medical student and now his
book will help others overcome their phobia. He has distilled
a large volume of information to present a coherent structure
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for ‘thinking neurologically’. A few secure principles go a long
way in neurology and they’re all here. Happy flying!
Martin R Turner
Consultant Neurologist
John Radcliffe Hospital
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Oxford, UK
Richard & Joan Doll Clinical Tutorial Fellow
Green Templeton College
University of Oxford, UK
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January 2012
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Preface
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ous, difficult and therapeutically nihilistic by many medical
students and non-neurologist physicians. Although there is
no doubt that the examination of the nervous system is an
involved and detailed process, it only remains mysterious
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and difficult to those who do not bother to learn how to do it!
For many patients the management of neurological disease
remains supportive, but on many fronts there are exciting
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breakthroughs that keep the specialty at the boundaries of
emerging therapeutic strategies.
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Pocket Tutor Neurological Examination aims to strike a
balance between simplifying the neurological examination
to an accessible level, and being a clinically useful reference
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tool. Medical students should find in it enough detail to pass
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examinations with confidence, and junior doctors should find
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enough detail to feel confident in examining patients with acute
neurological signs and symptoms.
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Chapters 1–5 cover the core examination techniques that are
essential to every interaction with neurology patients. Chapters
6–8 cover less commonly required routines that will be used
when the remainder of the clinical assessment indicates more
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detailed examination in these areas. Chapters 9 and 10 cover
the assessment of the stroke and coma patient, respectively.
These chapters are included because such patients require an
adapted and targeted neurological examination. Students and
doctors should all be aware of how to approach these common
clinical scenarios with a specific and well-rehearsed routine.
Chapters 11 and 12 cover a screening neurological examina-
tion and the neurological examination in undergraduate finals.
Together these offer a final polished routine that can be used
in final examinations or for general assessment in routine
clinical practice.
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All clinical examination technique is perfected through prac-
tice, and this is particularly true of the neurological examination.
I hope this pocket book will serve as a guide and reminder as
you learn at the bedside.
John A Goodfellow
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January 2012
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Contents
Foreword v
Preface vii
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Acknowledgements xii
Chapter 1 Clinical skills in neurology
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1.1 The consultation 1
1.2 The neurological history 1
1.3 The neurological examination 4
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1.4 Case summary and synthesis 5
1.5 Presenting patients 6
1.6 The junior doctor’s neurology toolkit 6
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1.7 Ethicolegal considerations 7
Chapter 2 Gait and general inspection
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2.1 Anatomy and physiology review 9
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2.2 Clinical features and pathophysiology 12
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2.3 General inspection 16
2.4 Abnormal posture and movements 18
2.5 Assessing gait 22
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2.6 System summary 24
Chapter 3 Head and neck (cranial nerves)
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3.1 Objectives 27
3.2 Anatomy and physiology review 27
3.3 Clinical features and pathophysiology 38
3.4 General observations 49
3.5 The nose (CN I) 50
3.6 The eyes: part 1 (CN II and III) 52
3.7 The eyes: part 2 (CN III, IV, VI) 59
3.8 The face (CN V, VII) 62
3.9 The ears (CN VIII) 67
3.10 The mouth (CN IX, X, XII) 71
3.11 The neck (CN XI) 73
3.12 System summary 74
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Chapter 4 Upper limbs
4.1 Objectives 77
4.2 Anatomy and physiology review 77
4.3 Clinical features and pathophysiology 85
4.4 General observations 88
4.5 Tone 89
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4.6 Power 90
4.7 Reflexes 96
4.8 Co-ordination 98
4.9 Sensation 99
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4.10 System summary 103
Chapter 5 Lower limbs
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5.1 Objectives 105
5.2 Anatomy and physiology review 105
5.3 Clinical features and pathophysiology 109
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5.4 General observations 111
5.5 Tone 112
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5.6 Power 112
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5.7 Reflexes 117
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5.8 Co-ordination 119
5.9 Sensation 120
5.10 System summary 124
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Chapter 6 Cerebellum
6.1 Objectives 125
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6.2 Anatomy and physiology review 125
6.3 Clinical features and pathophysiology 127
6.4 General observations 128
6.5 VANISHD 129
6.6 System summary 134
Chapter 7 Higher cortical function
7.1 Objectives 135
7.2 Anatomy and physiology review 136
7.3 Clinical features and pathophysiology 138
7.4 Bedside testing of cognitive domains 141
7.5 System summary 148
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Chapter 8 Autonomic nervous system
8.1 Objectives 151
8.2 Anatomy and physiology review 151
8.3 Clinical features and pathophysiology 155
8.4 History 156
8.5 Bedside examination and tests 157
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8.6 System summary 159
Chapter 9 Examining the stroke patient
9.1 Objectives 161
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9.2 Anatomy and physiology review 161
9.3 Clinical features and pathophysiology 163
9.4 Stroke history 167
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9.5 Stroke neurological examination 169
9.6 Stroke general examination 171
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9.7 Thrombolysis 172
9.8 System summary 173
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Chapter 10 Examining the coma patient
10.1 Objectives 175
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10.2 Anatomy and physiology review 175
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10.3 Clinical features and pathophysiology 175
10.4 General observations 178
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10.5 Eyes and reflexes 180
10.6 System summary 182
Chapter 11 The neurological screening
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examination in 4 minutes
11.1 Objectives 185
11.2 Sequence 185
Chapter 12 The neurological examination
in undergraduate exams
12.1 Objectives 187
12.2 Common conditions in examinations 188
12.3 Examination instructions 188
12.4 Questions and answers 189
Further reading 191
Index 193
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Acknowledgements
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Thanks to Paul Mayhew and Richard Furn at JP Medical for their
guidance, enthusiasm and patience. Thanks to Neel Burton for
taking time out from his own writing to review the manuscript
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and offer crucial advice. Thanks to Martin Turner for writing the
foreword in the midst of busy clinical and research commit-
ments. Thanks to Jakub Scaber for all the helpful neurology
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discussions.
Thanks to my wife, Rosalyn, for her support, encouragement
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and enthusiasm.
Thanks to the neurologists and neurosurgeons who have
taught and inspired me over the years: Professor Hugh Willison,
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Dr Martin Turner, Professor Kevin Talbot, Dr David Hilton-Jones,
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Dr Margaret Esiri, Professor Angela Vincent, Dr Saif Razvi, Dr
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George Gorrie, Dr Krishna Dani, Mr Edward St George, Mr Mario
Teo, Miss Emer Campbell and the whole team at the Institute
of Neurological Sciences in Glasgow.
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From the publisher
The photos used in figures 3.5, 3.6 and 4.1 were originally pub-
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lished in Pocket Tutor Surface Anatomy (© 2012 JP Medical Ltd)
and are reproduced courtesy of Sam Scott-Hunter, London, UK.
xii
chapter
Clinical skills 1
in neurology
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1.1 The consultation
The majority of clinical neurology is practised in the outpatient
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setting, usually by consultants or registrars. However, neuro-
logical emergencies and chronic neurological conditions are
common enough that every junior doctor needs to be skilled
in their assessment and key areas of management.
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The key clinical skill in neurology is history taking. This stage
will almost always be the most informative, and time well spent
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here will make the rest of the consultation more meaningful.
The history and other areas of the consultation enable the le-
sion to be localised and likely pathological processes identified.
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Rather than the history, the physical examination is the
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part that most inexperienced juniors are nervous about and
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likely to spend most time on. The value of the examination is
in confirming abnormalities suspected from the history and
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in detecting dysfunction not reported by the patient, thereby
further assisting in localising the lesion. If the history is taken
properly, there should be no surprises!
Investigations should be considered as an extension of
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the physical examination, that is, to confirm or refute specific
findings from the history or examination. Many patients who
consult a neurologist expect a brain scan, but this is not always
in their interest; most patients can be reassured by nothing
more than a thorough history and examination.
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Meeting the patient
When first meeting the patient:
• ask their name, age, handedness and employment history
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• establish rapport
Presenting complaint
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To determine more about the presenting complaint, ask an
open question to identify the patient’s main concern, such as
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‘What is the main problem?’ If there are multiple problems,
approach them separately and in turn.
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History of presenting complaint
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For each problem establish:
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• the time of onset: ‘When were you last well in this regards?’
• progression: ‘How has it changed since it started?’
• relation to other symptoms: ‘Which came first? Then what?’
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• time course
• aggravating and relieving factors
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Time course
Establishing the time course of symptoms is crucial but easily
passed over. Determine as exactly as possible the day, week
or month of symptom onset, the order of onset of symptoms
and their progression.
The differential diagnosis of neurological conditions is
greatly influenced by whether the symptoms are acute, sub-
acute or chronic.
• loss of consciousness
• abnormal movements
• headaches
• weakness
• sensory symptoms
• balance problems
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• visual problems
• seizures
• speech problems
• memory or planning problems
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• skin problems
• infections
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Past medical history
When taking the past medical history:
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• establish all previous med-
ical and surgical problems
• include any childhood ill-
Clinical insight
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nesses Always clarify what a patient means
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• clarify dates and precise when they use medical jargon or
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diagnostic terms. They may mean
meanings of any medical something completely different from the
terms the patient uses established meaning!
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Social history
This is an important element. Ensure a full history is taken,
including:
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• employment history (‘What age were you when you left
school?’, ‘What was your first job?’, ‘What was your next?’,
etc.), including occupational exposure to chemicals and
other potential hazards
• travel history
• unusual diet
• smoking and alcohol history
• recreational drug use
• human immunodeficiency virus and other blood-borne virus
risk factors
• where the patient lives and with whom
• levels of stress at home and at work
4 Clinical skills in neurology
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taking, and is usually perceived as such other major illnesses
by the patient. It also makes it easier to
return to discussing these topics if they
are subsequently thought to be important Drug history
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A full drug history should be
contributors to the presenting problem
(e.g. psychogenic pseudoseizures).
taken. The current or past
use of antidopaminergic
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drugs should be documented in patients with movement
disorders.
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Systems review
Thorough questioning about other systems should be carried
out:
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• include cardiac, renal, respiratory, gastrointestinal, psychi-
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atric and ophthalmological symptoms as standard
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• ask yourself whether the neurological disease is contribut-
ing to the systemic symptoms, whether disease of another
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system is contributing to neurological symptoms or whether
there is an underlying multisystem disease
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At the end of the history there should be a number of neurologi-
cal symptoms detected and a range of differential diagnoses to
account for them. The subsequent examination will be either a
brief screening examination or a more thorough assessment. A
succinct screening exam is appropriate when the likelihood of
signs is low (e.g. in patients with suspected simple migraine),
whereas a detailed assessment is appropriate if the differentials
include disorders likely to have physical signs, for instance, in
patients with suspected myasthenia gravis.
Patients sometimes find the neurological examination to be
a strange experience, with a doctor asking them to obey odd
Case summary and synthesis 5
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in the rest of their body.
The remaining chapters describe the various parts of the
examination. With experience, it becomes easier to decide
how detailed an exam needs to be and how to focus the exam
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according to the differentials. For example, in acute stroke, a
brief but targeted screening examination (see Chapter 9) allows
classification of the stroke syndrome, which is important for
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immediate management decisions, but does not delay treat-
ment by searching for minor neurological signs. In contrast,
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patients with Guillain–Barré
syndrome need detailed Clinical insight
assessment of all peripheral
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How to summarise a case
nerves to enable close moni- Suspected multiple sclerosis: example
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toring of progression. case summary
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A 27-year-old, female, right-handed
1.4 Case summary supermarket worker presents with a
2-week history of slowly progressive
and synthesis
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paraesthesias in both legs. Her past
medical history includes an episode of
The neurological case is often transient right visual loss 2 years ago, and
lengthy and detailed in terms a 2-week episode of acute ataxia and
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of the complete history and vertigo 6 months ago. Examination reveals
examination findings. It is a sensory loss of pin prick to her skin to the
region of the T10 dermatome, clonus in
helpful to routinely sum- both ankles and brisk knee reflexes. There
marise the relevant positive is no family history of multiple sclerosis or
and negative findings when other neurological disease.
writing in the case notes. This Opinion: multiple sclerosis seems
a likely diagnosis. Other causes of
step helps to clarify the case
demyelination need to be excluded.
and synthesise the various Plan: MRI brain and spinal cord; lumbar
elements. It should come af- puncture for cell count, protein and
ter the examination findings glucose, and oligoclonal bands; consider
and consist of just a para- visual-evoked potentials if the above is
not diagnostic.
graph or two of the findings.
6 Clinical skills in neurology
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ing task because of the often complex history and examina-
tion findings. The key is having thought through the case and
being clear what the relevant positive and negative findings
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are. It is helpful to start the case presentation or referral with
a brief summary that highlights the working diagnosis and/or
management plan. For example, in a patient with suspected
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myasthenia gravis, it would be helpful to begin with:
This 35-year-old right-handed man with no past medical
history presents with facial, bulbar and proximal limb weakness
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that is consistent with myasthenia gravis.
In an examination situation the examiners may simply allow
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students to proceed to describe the usual history and examina-
tion findings. However, since you have already clearly identified
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and summarised these, the impressed examiner may in fact skip
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this altogether and ask about investigation and management,
thereby allowing more advanced discussion.
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When referring patients to neurologists, for example over
the phone, it is helpful to begin with a brief summary or back-
ground such as the above. This shows that the patient has been
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carefully assessed and allows the neurologist to see where the
referral is going from the outset.
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• tuning forks for vibration sense testing (assessing the dorsal
columns)
• pins for pin-prick testing (assessing the lateral columns)
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• a few small objects (e.g. key, battery) are good for assessing
stereognosis
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• tongue depressors and throat swabs are helpful when the
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gag reflex needs to be formally tested
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It is also useful to carry a Snellen pocket chart for testing
acuity and to use Ishihara plates, e.g. on a smartphone, when
indicated. A variety of tools are available for bedside screening
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of cognition. For example, the Queen Square Screening Test for
Cognitive Deficits is a small book available directly from the Na-
tional Hospital for Neurology and Neurosurgery in London for
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£10 (€12). The Addenbrooke’s cognitive examination is a shorter
alternative, freely available online (http://www.stvincents.ie/
dynamic/File/Addenbrookes_A_SVUH_MedEl_tool.pdf )
Driving restrictions
There are driving restrictions for those diagnosed with certain
neurological disorders, and such a patient should be referred
to the relevant public authority (e.g. the Driver and Vehicle
Licensing Agency (www.dvla.gov.uk) in the UK) for up-to-date
details on driving restrictions. Some patients will be eligible
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for disability welfare support (e.g. Disability Living Allowance
(DLA) in the UK).
Expectations of imaging
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Many patients expect or want some form of neuroimaging for
reassurance. Although it is now relatively straightforward to
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obtain this for almost any neurological symptom, it is impor-
tant to discuss a number of issues with patients. CT scanning
involves radiation exposure and is not, strictly speaking, a
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harmless investigation.
MRI avoids this but often identifies incidental abnormalities
that are unrelated to the presenting problem and of uncertain
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significance. This occurs in around 10% of scans and is a major
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consideration in the design and implementation of neuroim-
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aging research studies that utilise ‘normal’ controls. As well as
increasing anxiety in patients, there may also be health and
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travel insurance implications.
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chapter
Sensory input
The dorsal column–medial lemniscus pathway carries
proprioceptive input from the joints and muscles in the
periphery to the dorsal column of the spinal cord. It ascends
ipsilaterally to the level of the medulla, where the primary
sensory neurons synapse on secondary neurons in the cuneate
and gracile nuclei (see Figure 4.3). These then decussate (the
internal arcuate fibres) and ascend as the medial lemniscus to
synapse on neurons in the ventral posteromedial and ventral
posterolateral nuclei in the thalamus. From here there are
diffuse projections, most importantly via the internal capsule
to the primary sensory cortex (the postcentral gyrus).
10 Gait and general inspection
• substantia nigra
• subthalamic nucleus
Their inputs, internal connections and output pathways
are very complex (Figure 2.1). A detailed knowledge is
not required for clinical practice except in the rare cases of
small unilateral lesions and for functional neurosurgery for
movement disorders. The clinical syndromes that are caused by
basal ganglia dysfunction are
classified on clinical grounds Clinical insight
rather than on anatomical
Hemiballismus is an involuntary
localisation of the lesions.
flinging movement of a limb, most
The basal ganglia affect commonly seen in stroke patients.
cognition, emotion and, in It is usually caused by a lesion in the
particular, movement. They are contralateral subthalamic nucleus. The
involved in selecting individual lesion reduces the excitatory input to the
globus pallidus from the subthalamic
actions and motor plans. They nucleus. This in turn disinhibits the
are therefore at the centre thalamus, which thereby increases its
of motor function, between excitatory output to the cortex, resulting
planning and execution. in the hyperkinetic movements. It is a
loss of descending inhibition.
Cerebellum
There are more neurons in the cerebellum than in the rest of the
brain. The cerebellum is located in the posterior fossa and forms
the roof of the fourth ventricle. It is covered in more detail in
Chapter 6. Briefly, its chief function is the execution and control
of fine movements, ensuring proper timing and accuracy in
particular. It is a major site for the control of learned or automatic
movements. It can be thought of as a massive switchboard,
connecting incoming cortical and basal ganglia movement
plans with the cerebellar output nuclei, which in turn project
back to the spinal cord, vestibular nuclei and cerebral cortex.
It comprises two cerebellar hemispheres connected by the
vermis. The flocullonodular lobe is tucked in at the base. There
is somatotopic organisation with the head represented on the
anterior lobe, the upper limbs and upper trunk more posteriorly
and the lower limbs and lower trunk more posteriorly still. The
midline of the body is represented on the vermis and the distal
limbs laterally.
12 Gait and general inspection
Cortex
Thalamus Striatum
Subthalamic
nucleus
Globus
pallidus
externa
Substantis Substantia Globus
nigra pars nigra pars pallidus
reticulata compacta interna
Figure 2.1 Basal ganglia connections. Dopaminergic input from the substantia
nigra and input from the motor cortex are modulated as they pass through the
pallidum and back into the thalamus and cortex. There are separate, parallel,
direct and indirect loops through the GPi and GPe/subthalamic nuclei back to
the thalamus and cortex. GPe, globus pallidus external; GPi, globus pallidus
internal; SNr, substantia nigra pars reticulata; SNc, substantia nigra pars compacta
Non-neurological disease
Manifestations of cardiac, respiratory, endocrine or gastrointestinal
disease may be evident on general inspection. Do not overlook
these as they may provide clues to the underlying aetiology of
any neurological deficits.
Pronator drift
One arm will slowly pronate when the arms are in front and the
eyes closed. This is a quite sensitive marker of an upper motor
neuron lesion in the corticospinal tract.
Abnormal posture
Abnormal postures may indicate distinct patterns of weak
ness:
• pyramidal distribution of weakness: there is greater
weakness in the arm extensors than in the flexors, leading
to a flexed elbow and wrist. This indicates an upper motor
neuron lesion, e.g. cortical stroke
14 Gait and general inspection
Abnormal movement
Movements may be reduced or excessive. Reduced movements
include bradykinesia, which is a slowness or lack of movement.
This is the hallmark of akinetic–rigid syndromes such as
parkinsonism. Additional (excessive) movements include
tremor, which is an involuntary rhythmic oscillation of a body
part. It can be physiological or pathological, and is classified as a:
• resting tremor: present at rest, but may be exacerbated with
distraction, e.g. Parkinson’s disease
• action tremor
• psychogenic tremor: common. Usually it is variable,
distractible, occurs inconsistently and may be entrainable (i.e.
when the patient is asked to tap another limb at a different
frequency from the tremor, the limb with the tremor then
oscillates at the new frequency)
Action tremors There are several different types of action tremor:
• postural: occurs when maintaining a posture, e.g. essential
tremor, renal or liver disease
• kinetic: occurs during a voluntary movement
• intention: occurs at the end of target-directed movements,
and is caused by cerebellar lesions
• task specific: occurs during specific tasks such as writing or
playing a musical instrument
Clinical features and pathophysiology 15
Gait
The gait can be broadly symmetrical or asymmetrical, and
generally broad- or narrow-based. The patient may have
difficulty initiating movements or turning.
feet at all. They will tend to veer towards the side of the
lesion
• peripheral nerve sensory lesions cause a similar wide base, but
patients may lift and slap both their feet more prominently
Narrow-based These include:
• Parkinsonism usually presents with a slow shuffling gait.
Patients are stooped forward and have a reduced arm swing.
They struggle to initiate movements and take several steps
to turn
• diffuse vascular disease may cause the marche à petits
pas (march of a thousand steps, literally, ‘walking with very
small steps’), in which the narrow-based shuffling gait is
accompanied by a more upright posture
• a myopathic gait appears waddling as there is weakness in
the proximal muscles
Asymmetrical gait
An asymmetrical gait can result from a wide range of problems:
• the hemiplegic gait is narrow based, although the affected
leg will swing out to the side with a tilting movement of the
hip during the movement
• foot drop: weakness of tibialis anterior from any cause will
result in reduced ankle dorsiflexion and the characteristic
floppy foot. Causes include L5 radiculopathy, common
peroneal palsy and a cingulate gyrus lesion
• magnetic gait: this describes gait apraxia, in which the
patient seems stuck to the floor. Causes include stroke and
normal pressure hydrocephalus
Approach
Patients strip to their undergarments, having been warned that
they will be inspected closely.
Sequence
Use the following sequence:
1. ask the patient to undress, but to keep on their underwear
2. inspect the patient from front and from behind, noting the:
• posture
• skin colour, pigmentation, lesions, naevi
• muscle bulk, wasting, fasciculations
Approach
Observe the gait without explicitly warning the patient as this can
cause them to either involuntarily suppress abnormal movements
or to manifest functional signs. Instead, during the history–taking
part of the assessment, try to note any abnormal movements.
To further assess abnormal movements and to elicit latent
signs, patients are usually asked to perform some specific tasks.
Equipment
For this part of the examination, pen and paper are required.
Sequence
The following sequence is used to assess abnormal movements
and to elicit latent signs:
1. when taking the history, note whether there are any abnormal
movements. Start at the patient’s head and work down
looking for a lack of movement or additional movements
2. note whether there is a general poverty of movement (i.e.
reduced blink rate, hypomimia, slowed speech)
3. note:
• facial movements and head position
• arm positions and movements
• leg positions and movements
• any resting tremor
4. ask the patient to hold their hands out straight in front of
them with their fingers spread out. Note any tremor
5. ask them to cock their wrists back and hold them there.
Observe for asterixis
6. ask them to lift their arms out to the side and bring their
fingertips together in front of their nose by bending their
elbows and to hold that position (Figure 2.2). Note any
dystonic posture or tremor
7. ask them to touch their forefinger to their thumb and to
open and close that as fast and as fully as they can. Note
any slowed speed or decreased amplitude
8. ask them to write a sentence and draw a spiral. Note any
micrographia or oscillations that indicate a tremor
20 Gait and general inspection
9. assess tone in their upper limbs (see Chapter 4), noting any
cogwheeling or rigidity
Table 2.1 Comparison of the tremor of Parkinson’s disease and essential tremor
22 Gait and general inspection
Approach
Observe the patient walking and performing a few movements.
Equipment
No equipment is required for this part of the examination.
Sequence
The following sequence is used:
1. ask the patient to stand as able
Assessing gait 23
2. ask them to put their feet together and close their eyes.
Ensure they do not fall. This is Romberg’s test. If the patient
sways markedly and loses their balance, the test is positive
and indicates loss of proprioception
3. ask the patient to walk to the other end of the room. Observe
the stride length, pattern, width of base, dorsiflexion of the
ankle, speed, turning and arm swing
4. ask them to turn and come back
5. ask the patient to walk away again, heel to toe; if they manage
this, have them walk heel
to toe backwards Clinical insight
6. ask the patient to walk on
Examining shoes in patients with
their toes, then their heels abnormal gait can be informative:
7. ask them to squat down • worn-in shoes are good indicators
and stand up without of the usual gait pattern and may
touching the floor confirm that the observed abnormal
gait has been consistently present for
8. test for retropulsion by some time
standing behind them and • shoes with a normal pattern of wear
pulling their shoulders may suggest the gait dysfunction is
towards you. See how intermittent. This does not exclude
many steps they take to organic pathology but could suggest
a functional disorder or deliberate
steady themselves, but do malingering
not let them fall
Table 2.2 The key aspects of general inspection and examining the gait
chapter
3.1 Objectives
Examination of the cranial nerves is a vital skill for students and
junior doctors. The principles are identical to any other portion
of the neurological examination but many students and physi-
cians find this part daunting. It need not be so.
This chapter is on the ‘head and neck’ rather than on ‘cranial
nerves’ to remind the clinician that the neurological assessment
includes not only the nerves themselves but also the whole
neuroaxis from the muscle or sensory endings, neuromuscular
junction, peripheral cranial nerve fibres and brainstem nuclei
to the higher centres.
As with other parts of the examination, the key principles
are to:
• detect abnormal signs
• localise any lesions
• identify potential pathogenic processes.
Cranial nerve Motor innervation Sensory input Autonomic component Brainstem nuclei
IX Glossopharyngeal Stylopharyngeus muscle Pharynx and posterior 1/3 Parasympathetic Motor in medulla
of the tongue secretomotor fibres to the Parasympathetic in pons
parotid
X Vagus Muscles of larynx, Larynx Parasympathetic Motor, sensory and
pharynx and palate Portion of external innervation of bronchi, parasympathetic in
involved in speech auditory meatus bronchioles, atria of medulla
Viscerosensory from heart, liver, gallbladder,
gastrointestinal tract, pancreas, oesophagus,
lungs, heart and aortic stomach, gut (to colonic
arch flexure) and kidneys
Head and neck (cranial nerves)
CN I Olfactory
CN II Optic
CN III Oculomotor
CN IV Trochlear
CN VI Abducens CN V Trigeminal
(ophthalmic branch)
CN VII Facial
(Maxillary nerve)
CN IX
Glossopharyngeal (Mandibular nerve)
CN X Vagus CN VIII
Vestibulocochlear
CN XII Hypoglossal CN XI Accessory
a
f
Scotoma
Unilateral visual loss
b
Bitemporal hemianopia g
a f Unilateral nasal hemianopia
g
c h
Homonomous hemianopia b
Head and neck (cranial nerves)
h
Homonomous superior quadrantonopia
d c
Homonomous inferior quadrantonopia i
d i
Homonomous hemianopia
e
Homonomous hemianopia e
(with macular sparing)
Pupilliary muscle
Retinal
ganglion cell
Ciliary ganglion
Portion of the
oculomotor nerve
Superior
colliculi
Edinger-Westphal
nuclei
Afferent limb Midbrain
Efferent limb
Figure 3.3 The pupillary reflex arc involves CN II (afferent limb; grey) and CN III
(efferent limb; blue) at the level of the midbrain
Figure 3.4 Primary direction of action of muscles involved in the control of eye
movements
34 Head and neck (cranial nerves)
V2
V3
C2
Light reflex
The afferent limb of the light reflex consists of the retina,
optic nerve, optic chiasm, optic tract, superior colliculus and
Edinger–Westphal nuclei in the midbrain. The efferent limb
consists of the Edinger–Westphal nucleus, preganglionic
Anatomy and physiology review 37
Cranial root
Foramen magnum
Jugular formen
Spinalroot
Innervation of
sternocleidomastoid Innervation of trapezius
Figure 3.8 Accessory nerve. The spinal roots pass up through the foramen
magnum and join the cranial root, which then branches off to run with the vagus
nerve. The remainder forms the main body of the accessory nerve and innervates
the trapezius and sternocleidomastoid muscles
Accommodation reflex
A normal accommodation reflex is for the pupils to constrict
as the patient focuses on near vision. The afferent limb of this
reflex begins with the frontal eye fields in the frontal lobes,
rather than the optic nerve. The efferent path is the same as
the light reflex.
CN II
Swollen optic disc
This is an elevated disc with blurred margins, venous engorge-
ment and loss of venous pulsation.
Pathophysiology This results from either papilloedema or
papillitis:
• papilloedema: swollen disc caused by raised intracranial
pressure; pressure on the retinal vessels and nerves can
cause irreversible loss of vision (late)
• papillitis: swollen disc caused by inflammation; Retinal or
optic nerve inflammation causes acute visual loss (early) and
pain on moving the eyes
Pale disc
A pale white colour suggests optic atrophy from any cause.
Pathophysiology The causes of a pale disc include retinal
or nerve head ischaemia or a chronic phase of optic neuritis
leading to degeneration of the retinal ganglion cells.
Diabetic retinopathy
There is rubeosis (blood vessel formation over the iris), cataracts
and other key features:
• proliferative changes: new blood vessel formation,
haemorrhages, scars, retinal detachment
Syndrome Cranial nerves Location of lesion Typical causes Clinical features
involved
Bell’s palsy VII VII nerve Idiopathic Unilateral lower motor neuron facial nerve
weakness, hyperacusis, loss of taste, dry eyes
Tolosa–Hunt III, IV, VI (V1) Polyneuropathy Idiopathic inflammation Unilateral orbital pain over weeks
syndrome
Cavernous sinus III, IV, VI (V1) Cavernous sinus Carotid dissection, carotid Progressive ophthalmoplegia, painful
syndrome aneurysm, thrombophlebitis of diplopia, exophthalmos
sinus, infection of sinus
Ramsay–Hunt VII (V) VII nerve Herpes zoster Acute unilateral facial palsy following ear pain
syndrome with vesicles in auditory meatus
Jugular foramen IX, X, XI Jugular foramen Glomus tumour, meningioma, Unilateral hoarseness, loss of gag
syndrome acoustic neuroma, metastases, reflex, uvula deviates, dysphagia,
trauma sternocleidomastoid and trapezius weakness
Cerebellopontine V, VII, VIII Cerebellopontine Acoustic neuroma, lipoma, Hearing loss, tinnitus, vertigo, facial numbness
angle angle vascular malformation, metastases
Bulbar palsy Bilateral lower Nuclei of affected Guillain–Barré syndrome, motor Dysphagia, dysarthria, loss of gag reflex,
motor neuron X, nerves or peripheral neuron disease, sarcoidosis tongue fasciculations
XI, XII nerves
Pseudobulbar Bilateral upper Corticobulbar Motor neuron disease Dysphagia, dysarthria, exaggerated gag
palsy motor neuron X, tracts, supranuclear and jaw reflex, pseudobulbar affect, slow
Clinical features and pathophysiology
Lateral pons V, VII, VIII Lateral pons AICA CL: loss of sensation on body
IL: limb ataxia, facial weakness, Horner syndrome,
deafness, tinnitus
Vertigo, nystagmus
Weber III, VII Midbrain peduncle PCA CL: face, arm and leg weakness
syndrome IL: medial rectus weakness, mydriasis
Impaired vertical gaze
Midbrain III Midbrain PCA CL: limb ataxia, choreoathetosis, hemiballism
tegmentum tegmentum IL: medial rectus weakness, mydriasis
Impaired vertical gaze
Table 3.5 Brainstem syndromes. AICA, anterior inferiorcerebellar artery. CL, contralateral. IL, ipsilateral. INO, internuclear ophthalmoplegia. PCA,
posterior communicating artery. PICA, posterior inferior cerebellar artery. PP, pin prick sensation. Temp, temperature sensation. Vib, vibration sense
Clinical features and pathophysiology 41
Hypertensive retinopathy
This is graded as shown in Table 3.7.
Pathophysiology This results from systemic hypertension,
which causes accelerated arterial sclerosis and the above
changes. Changes can occur slowly with chronic hypertension
or acutely with malignant hypertension.
Stage Features
1 Non-proliferative/background retinopathy: microaneurysms, hard
exudates, dot–blot haemorrhages
2 Maculopathy: changes occur in the macula
3 Proliferative retinopathy: neovascularisation, vitreous
haemorrhages, retinal detachment
Grade Features
1 Silver wiring (sclerotic vessels appear silvery)
2 Grade 1 plus marked deflection of veins as they cross arteries
(arteriovenous nipping)
3 Grade 2 plus flame haemorrhages and soft and hard exudates
4 Grade 3 plus papilloedema
Hemianopia
This is a loss of a portion of the visual field. It differs from retinal
scotomas in that the defect persists when either eye is closed
in turn.
Pathophysiology Figure 3.2 elaborates on localising visual
field defects. In general, a homonymous hemianopia indicates
a retrochiasmal lesion.
Pupils
Dilated pupil
This results from a failure to constrict to light. The following
can be distinguished:
• normal accommodation: relative afferent papillary defect
(RAPD) (i.e. retinal or optic nerve disease; Figure 3.9)
• slow accommodation: Holmes–Adie pupil
• failure of accommodation: IIIrd nerve palsy or drug effect.
Pathophysiology RAPD results from a failure to stimulate the
light reflex owing to retinal or optic nerve pathology, such
as optic neuritis in multiple sclerosis. The pupil will constrict
when light is shone in other eye. A Holmes–Adie pupil is
tonically dilated from degeneration of the ciliary ganglion. It
will accommodate slowly. A IIIrd nerve palsy will cause ptosis
and the eye will be ‘down and out’. If there is a ‘surgical cause’
Clinical features and pathophysiology 43
Constricted pupil
This results from a failure to dilate in low light. The following
can be distinguished:
• unreactive to light with normal accommodation: Argyll
Robertson pupil
• unreactive to light with no accommodation: likely drug effect
• small with a sluggish reaction to light is common in elderly
(senile meiosis)
• small, sluggish, ptosis, anhidrosis: Horner’s syndrome
Pathophysiology Senile meiosis is a common cause. Argyll
Robertson pupils are rare but indicate a midbrain lesion; causes
include diabetes and syphilis. Horner’s syndrome is caused by
a lesion in the sympathetic supply to the eye, causing tonic
constriction. Lesions can be in the hypothalamus, medulla,
cervical cord, superior cervical ganglion or carotid artery. Stroke
is a common cause in the central nervous system; a Pancoast’s
tumour in the apex of the lung is an important peripheral cause.
In young people, it suggests carotid artery dissection.
44 Head and neck (cranial nerves)
CN III, IV, VI
Ptosis
Ptosis is weakness of the levator palpebrae superioris (eyelid
muscle), resulting in drooping of the eyelid. It can be partial,
full, unilateral or bilateral.
Pathophysiology This can be:
• bilateral, in which there is likely to be primary muscle or
neuromuscular junction disease (e.g. myopathy, myasthenia
gravis)
• unilateral, owing to a lesion of the IIIrd nerve or nuclei.
If painful, the eye is ‘down and out’ and the ptosis is
accompanied by a large unreactive pupil, assume that
there is an expanding aneurysm until proven otherwise.
Diabetic infarction of the IIIrd nerve may spare the pupil
Tilted head
The patient holds their head at an angle to avoid diplopia. This
may be subtle and the patient may not be aware of it.
Pathophysiology The patient’s posture can be indicative as
the head tilts away from the side of the affected IVth nerve.
This compensates for the failure of the superior oblique to
intort the eye.
CN V
Absent corneal reflex
This is a failure of the blink reflex on stimulation of the cornea.
Stimulation on one side should normally provoke blink on both
sides.
Pathophysiology This is due to a lesion in CN V, which will cause
loss of the afferent limb of the reflex arc with the loss of blink
on the affected side and on the contralateral side. The efferent
limb of the arc is mediated by the VIIth nerve. A lesion in the
VIIth nerve results in the loss of blink on the affected side but
preserved blink on the contralateral side.
46 Head and neck (cranial nerves)
Trigeminal neuralgia
This is a brief stabbing, shooting, electric shock-like pain in the
distribution of the trigeminal nerve. It is provoked by touching
the face, chewing or drinking.
Pathophysiology The neuralgia is caused by a lesion in the
trigeminal nerve or nuclei. It can be idiopathic or it can be
secondary to an ectatic superior cerebellar artery irritating the
trigeminal nerve root.
CN VII
Clinical insight Facial asymmetry
Patients with Bell’s palsy frequently In facial asymmetry, there is
perceive themselves as having the
abnormality on the opposite side of a flattened nasolabial fold,
the face to the one actually affected. downturned mouth and there
An examining doctor may be led astray may be weakness of the eyelid
by listening to the patient telling them and a loss of forehead wrinkles.
which side is affected. Patients also
often report a subjective change in Pathophysiology This is
facial sensation, despite the Vth nerve caused by unilateral cortical
not being involved and a normal Vth
nerve examination. This may be due to
lesions (e.g. stroke), which
a change in muscle tone with the facial spare the forehead and eyelid
nerve palsy. as the brainstem nuclei to
Always record what you see as well as these receive bilateral cortical
what the patient says – even when they inner vation. Unilateral
do not agree.
brainstem or lower motor
neuron (LMN) lesions involve
the forehead and eyelid. Bell’s palsy (idiopathic inflammation of
the facial nerve) is usually dramatic in the apparent weakness.
Clinical features and pathophysiology 47
CN VIII
Conductive hearing loss
There is a subjective loss of hearing on the affected side. No vi-
bration is heard in the affected ear when a tuning fork is moved
in front of the ear in Rinne’s test (Rinne negative). Vibration is
heard louder in the affected ear in Weber’s test.
Pathophysiology In the presence of middle or external ear
pathology (e.g. wax), this results from air conduction in front
of the ear in Rinne’s test not being transmitted to the cochlear
nerve, but conduction through the skull is better so is heard
better in the affected ear.
Sensorineural deafness
There is subjective hearing loss on the affected side, vibration
is heard in the affected ear when the tuning fork is moved in
front of the ear in Rinne’s test (Rinne positive) and vibration is
heard louder in the unaffected ear in Weber’s test.
Pathophysiology This is caused by a lesion in the central
components of hearing (e.g. acoustic neuroma), which results
in failure of both air- and bone-conducted sound equally in
Rinne’s test and preservation of hearing in the normal ear in
Weber’s test.
CN IX, X
Displaced uvula
The uvula deviates towards the normal side on saying ‘Ah’ in
unilateral Xth nerve palsy.
Pathophysiology This results from a lesion in the vagus nerve
causing weakness of the muscles elevating the soft palate.
An intact contralateral vagus pulls the soft palate towards the
normal side. In bilateral lesions, the uvula will not elevate at all.
CN XI
Weakness of trapezius or sternocleidomastoid
Patients present with weakness of shoulder elevation
(trapezius) or head rotation (sternocleidomastoid muscle
turns the head away).
Pathophysiology Unilateral weakness indicates neck trauma
or a mass in the jugular foramen. Bilateral weakness indicates
generalised peripheral neuropathy, muscle disease or motor
neuron disease.
CN XII
Slow and spastic tongue
Patients have a small, immobile tongue; this may be associated
with dysarthria or dysphagia.
Pathophysiology There is an UMN lesion affecting the XIIth
nerve nuclei, which results in increased tone and weakness
of the tongue. It eventually wastes. Common causes include
motor neuron disease and stroke.
General observations 49
Wasted tongue
Unilateral LMN lesions of the XIIth nerve cause the tongue to
deviate towards the weaker side on protrusion. Wasting and
fasciculations occur secondary to denervation.
Pathophysiology Bilateral lesions can occur from motor neuron
disease or Guillain–Barré syndrome. Unilateral lesions result
from motor neuron disease, tumours in the cervical region or
lymphadenopathy.
Sequence
Use the following as a guide:
1. inspect the patient from the front and behind
50 Head and neck (cranial nerves)
2. look specifically for the features above and for any other
signs expected from the history
3. look for any scars, evidence of head injury or surgery to the
head or neck
4. test for neck stiffness
Approach
Formal testing is rarely performed or informative. However,
particularly after head injury, the loss of sense of smell can have
a significant impact on some patients and it is not infrequently
a source of compensation claims.
Equipment
No equipment is required for informal or screening assessment.
Three or four non-noxious smells should be presented to the
patient if formally testing smell, e.g. orange peel, coffee beans,
perfume and tobacco.
Sequence
Use the following sequence:
1. ask: ‘Any change in your sense of smell or taste?’
2. for more formal assessment, present three or four easily
recognisable scents to the patient (see above). Occlude each
nostril in turn and ask the patient if they (1) smell anything
and (2) recognise the smell
Objective
The objective is to assess the optic nerve and the parasympa-
thetic function of the oculomotor nerve.
Approach
Guiding principle Carry out this part of the
Avoid the temptation to rush assessment in a darkened
fundoscopy and pupillary responses room if possible. Inform the
and move onto eye movements. It is patient that they will have a
worth performing this stage properly as
bright light shone into their
it allows assessment of the optic nerve,
midbrain, thalamus (lateral geniculate eyes, which they may find un-
nucleus), internal capsule, and parietal, comfortable. Ask the patient
temporal and occipital lobes and can be to fixate on a distant object
very helpful in localising pathology. just above their head height.
Dilate the pupils if required.
Equipment
An ophthalmoscope, pen torch, Snellen chart, hat pin, Ishihara
plates and mydriatic drops are required.
Sequence
Pupils
To assess the pupils:
1. note the resting size, shape and symmetry of the pupils in
both dim and bright light
2. elicit the pupillary reflex in each eye in turn
The eyes: part 1 (CN II and III) (pupils, acuity, fields, fundi) 53
Acuity
To assess the acuity:
1. use a Snellen chart. Normal
acuity is ‘6/6’ (metres) or Clinical insight
‘20/20’ feet. ‘6/12’ vision A relative afferent pupillary defect
would represent the ability is when a pupil appears to dilate in
to read at 6 metres what response to moving a light from the
can usually be read at 12 other eye onto it. It is caused by any
damage to the retina or optic nerve
metres, i.e. reduced acuity on the affected side. This results in
2. if the patient is unable to the observation that when a light is
read the largest lettering shone in the other, unaffected, eye
on the chart, test if they the strong bilateral effector arm of the
pupillary response causes a contralateral
can: (a) see the number
constriction of the other pupil. This is
of fingers you are holding normal.
up; (b) see hand move- When there is damage to the retina or
ment; or (c) perceive light. optic disc, moving the light onto the
affected eye will result in less stimulation
Colour vision of the afferent limb of the reflex and the
pupil will dilate compared with when
Colour vision can be abnor- the light is in the other eye.
mal before acuity and should
also be tested with Ishihara
plates (an online, bedside version can be accessed at http://
colorvisiontesting.com/ishihara.htm) if there are any concerns
about vision.
Fields
Accurate assessment of any visual field loss helps to localise
a lesion along the optic pathway. Lesions at particular sites
along the pathway produce characteristic patterns of visual
loss.
54 Head and neck (cranial nerves)
Fundoscopy
To examine the patient’s fundi, ask them to remain fixated on
a distant point:
1. using the ophthalmoscope light, check the red reflex in both
eyes from a distance
2. use your right eye to examine the patient’s right eye and
your left eye to examine the patient’s left eye
3. with your eye at the same level as the patient’s, approach
from about 20° laterally with one hand on their head with
your thumb on the bony orbital margin of the eye you are
examining
4. approach their eye until the retina comes into focus. You
may need to get your head close enough that the ophthal-
moscope touches your finger on the patient’s orbit
5. identify an artery or vein and follow it back to the optic disc
6. examine the margins of the disc, checking that they are well
defined and that there is no swelling or cupping and note
its colour (an indistinct nasal margin is common)
7. examine the rest of the retina, taking each quadrant in turn
and specifically looking for features of diabetic or hyperten-
sive changes or any pigmentation
8. also note any signs of retinal detachment or artery or venous
occlusion or thrombosis
Ophthalmoscope adjustment The retina should come into
focus with the lens set at 0 and the optic disc at red 2. Black is
positive and focuses nearer; red is negative and focuses more
distant.
Removing spectacles for fundoscopy is preferred as it allows
closer examination but requires correction with the ophthalmo-
scope. Determine whether the patient is short or long sighted
and adjust the ophthalmoscope accordingly. If the examiner
also has a refractive error, it will either exaggerate the correction
required, if it is the same type of error as the patient, or partially
correct it, if it is the opposite. An approximate guide is to start
with the lens at +8, visualise the lens and anterior chamber of
the eye, and then move the lens down to 0 or below to bring
the fundus into focus.
56 Head and neck (cranial nerves)
Acuity
Rapid monocular visual loss The causes include:
• retinal artery or vein occlusion
• ischaemic optic neuropathy
• optic neuritis
• giant cell arteritis
• migraine
Rapid binocular visual loss The causes include:
• bilateral occipital lobe lesions (infarction, haemorrhage or
trauma)
• bilateral optic neuritis or papillitis (infection, inflammation
or infiltration)
• alcohol poisoning
• functional
Fundi
Optic disc The optic disc can appear swollen with a loss of normal
shallow cup and clear rim and blurring of margins or pale:
• bilaterally swollen is most likely papilloedema
• unilateral swelling can be due to optic neuritis or papillitis
• pale with normal margins,
caused by optic atrophy
Clinical insight from, for example, optic
Clinically, papilloedema usually does neuritis
not have severe visual loss until later on, • pale with deep margins in
whereas papillitis presents with early and
severe loss of visual acuity. glaucoma
Blood vessels Look for
arteriosclerotic and diabetic changes:
• arteriosclerotic changes: arteriolar narrowing, arteriove-
nous nipping (veins narrow as arteries cross them), silver
wiring, flame haemorrhages (bleeding into the nerve fibre
layer) and exudates
• diabetic changes: macular oedema, neovascularisation,
cotton wool spots (retinal infarcts) and flame or dot–blot
haemorrhages (Table 3.6)
Approach
There are three main types of clinically relevant eye movements:
pursuit, saccadic and vestibulo-ocular:
• the occipital lobes direct control of pursuit (the slow eye
movements used to track objects)
• the frontal lobes direct saccadic eye movements (the rapid
movements from points of fixation)
• the cerebellar vestibular nuclei control the vestibulo-ocular
movements (which maintain fixation during head move-
ments)
Saccadic eye movements are useful in finely localising
lesions but pursuit movements form the bulk of this stage of
the examination.
Ensure that you are directly in front of the patient at eye level
and that you give clear instructions and ask them to report the
development of any double
Clinical insight vision.
Patients with a head tilt often adopt
subtly unusual postures over time, to the Equipment
point where they may not realise they This part of the examination
have diplopia until they are asked to requires a hat pin and circular
straighten up.
card to cover each eye in turn.
Sequence
1. check the position of the patient’s head; straighten their
head if needed
2. check the resting position of the eyes
3. note any deviation, resting eye movements (Table 3.10) or
ptosis. Note whether they persist or worsen in each direction
of gaze
4. perform the cover test to detect latent strabismus. Cover
and then quickly uncover each eye in turn, having asked
Deviation Description
Skew deviation Eyes held in different vertical planes (i.e. one
higher than the other)
Strabismus Eyes not in alignment
Movement Description
Nystagmus Involuntary spontaneous movements. See
Chapter 6
Opsoclonus Rapid, unpredictable horizontal and vertical eye
movements
Saccadic oscillations Can be very small (benign) or larger
(pathological) back-to-back saccades
Ocular flutter Second saccade occurs in the opposite direction
after the main saccade
Square wave jerks Inappropriate saccades removing the eye from
its target, followed by refixation
Assessing saccades
To assess saccades, note whether the eyes move together in the
saccades and whether there are any abnormal movements at
the end of saccades. Abnormal movements such as nystagmus
and opsoclonus can be more evident at the end of saccadic eye
movements. An internuclear ophthalmoplegia may also be more
evident on saccades.
Internuclear ophthalmoplegia is a disorder of conjugate
gaze characterised by impaired adduction in the affected eye
and nystagmus in the abducting eye during lateral gaze or lat-
eral saccades. It is caused by a lesion in the medial longitudinal
fasciculus (MLF) ipsilateral to the eye with impaired adduction.
62 Head and neck (cranial nerves)
Equipment
This requires a cotton wool swab, a Neurotip, tuning fork,
universal containers with warm and cold water and a tendon
hammer.
Sequence
Inspect for:
1. wasting of the masseter or temporalis muscles
2. flattening of the nasolabial folds
The face (CN V, VII) 63
Table 3.11 Key eye movement disorders and differential diagnoses. MLF, medial
longitudinal fasciculus. PSP, progressive supranuclear palsy
64 Head and neck (cranial nerves)
CN V
After carrying out the initial inspection (above), assess CN V
as follows.
Assess sensory component Three main divisions each supply
a different portion of the head: the ophthalmic division, the
maxillary nerve and the mandibular nerve. Test each in turn
on both sides:
1. use a Neurotip (be gentle!) or the end of a clean paperclip
(if no Neurotips are available) to assess pain perception
2. other modalities are difficult to test as vibration tends to be
felt diffusely and proprioception is not really possible! Use a
universal container with warm and one with cold water to
test temperature if needed
3. touch the tip to the forehead (V1) on each side, asking the
patient whether it feels sharp and to compare the sensation
on both sides. Repeat just lateral to the cheekbones (V2) and
then either side of the chin (V3)
4. if an area of altered sensation is detected map it out in more
detail. Remember that the C2 dermatome begins near the back
of the head and the area below the angle of the jaw is also C2/3
and should be normal in lesions of the trigeminal nerve
Assess motor function To do this:
1. ask the patient to clench their teeth and feel the jaw for
muscle bulk
2. ask them to keep their mouth open while you attempt to shut
it. In unilateral lesions the jaw will deviate towards the weak side
3. test the jaw jerk. Ask the patient to loosely open their mouth
and place the tip of your thumb gently on their chin. Tap
your thumb on the joint softly with a tendon hammer to
elicit any jaw jerk
CN VII
Both motor and sensory functions of the facial nerve need to
be assessed.
The face (CN V, VII) 65
CN V sensory lesion
Table 3.12 shows likely lesion locations to account for common
types of CN V sensory loss.
Table 3.12 Trigeminal nerve sensory loss and likely location of lesions
Lower motor neuron lesions (e.g. Bell’s palsy) These will often be
fairly dramatic with full involvement of all the muscles, including
frontalis and orbicularis oculi, because the lesion is at the final
point of input to the muscle (i.e. the innervating motor neurons).
Bilateral lesions These may represent muscle disease rather than
nerve involvement, or be caused by Guillain–Barré syndrome,
sarcoidosis, Lyme disease or tuberculosis, although these are all
rare conditions. Other causes include tumours (including parotid
tumours), syrinx and multiple sclerosis. Trigeminal neuralgia
will cause paroxysms of intense electric shock-like pain in the
distribution of the trigeminal nerve.
Approach
Vestibular assessment is indicated if there are symptoms
suggestive of vertigo, dizziness, nystagmus, posterior
circulation involvement or a cerebellopontine angle lesion.
Gross auditory dysfunction may be evident from the history
taking. Specific symptoms or other findings may indicate more
detailed testing if a lesion is suspected.
Equipment
This part of the examination requires an otoscope and a 256- or
516-Hz tuning fork.
Sequence
To test the auditory nerve:
1. inspect the head and external ear for any scars, hearing
devices or local lymphadenopathy
2. inspect the internal auditory canal with the otoscope
3. visualise the tympanic membrane, which should be con-
cave, free from excessive wax and with a light reflex on the
anterior–inferior portion. Note any exudate or growth such
as a cholesteotoma
4. cover one ear and whisper a number in the other from about
60 cm away. Repeat on the other side
5. Rinne’s test and Weber’s test should be performed if there
are any reported symptoms or signs of hearing loss
Rinne’s test
Rinne’s test is performed as follows:
1. place the tuning fork on the mastoid process
2. when the patient cannot hear it, move it in front of the ear
on the same side
3. ask if they can hear the tone
4. vibration on the mastoid tests bone conduction
5. air conduction is tested when the tuning fork is in front of
the ear
Normally, the tone should be heard when the tuning fork is
moved in front of the ear (Rinne positive):
The ears (CN VIII) 69
Weber’s test
Weber’s test is performed as follows:
1. place the tuning fork on the centre of the patient’s forehead
2. ask if they hear it more in one ear
3. normally it is heard equally in both ears
4. with sensorineural loss, the tone is heard better in the unaf-
fected ear
5. with conduction loss, the tone is better heard in the affected
ear
Note whether they turn to one side on the spot. This indicates
a vestibular lesion on that side.
Deafness: conductive
Common causes of conductive deafness include wax, otitis
media and other middle ear disease.
Vestibular lesion
Important causes include labyrinthitis; toxins; vestibular
neuronitis; infarction or demyelination of nuclei or nerve; and
tumour at the cerebellopontine angle.
Objective
The purpose of this part of the examination is to assess the func-
tion of the lower cranial nerves. The IXth, Xth and XIIth cranial
nerves have similar origins, intracranial and initial extracranial
courses, and are commonly affected together.
Approach
Inform the patient that you will need to look in their mouth,
press down on their tongue and touch the back of their throat
and that they may find this uncomfortable.
Equipment
To carry out this part of the examination, a tongue depressor,
‘orange stick’ or throat swab, and pen torch are required.
Sequence
Carry out the following steps in turn:
1. ask the patient to open their mouth; inspect the palate and
tongue using a pen torch
2. note the position of the uvula and whether there is any
deviation (CN X)
3. look for fasciculations or wasting of the tongue (CN XII)
4. ask the patient to say ‘Ah’ and watch for elevation of the uvula
(CN X). This should be central. Unilateral lesions of the vagus
nerve will draw the uvula to the normal side and bilateral
lesions will result in no movement
5. ask them to protrude their tongue straight out (it will deviate
to the weak side) and then to move it back and forth; note
any stiffness or slowness (CN XII)
6. ask the patient to speak, noting any dysarthria (CN IX, X or
XII) or hoarseness (CN X)
7. have them cough (CN X) and swallow some water (CN IX, X
and XII)
72 Head and neck (cranial nerves)
8. test the gag reflex using the tongue depressor and the throat
swab. Touch the back of the pharynx on each side, observing
for a contraction of the soft palate. Ask the patient if they
felt the touch on each side
9. the afferent limb is carried by the sensory fibres of the glos-
sopharyngeal (CN IX) via the nucleus solitarius and the spinal
trigeminal nucleus. The efferent is carried by the motor fibres of
the vagus (X). Note an absence or exaggeration of the gag reflex
10. taste on the posterior third of the tongue can be tested to
examine the function of the CN IXth nerve; however, unless an
isolated CN IX lesion is suspected it is not commonly performed
Findings
Clinical insight Common findings are:
• dysarthria
Autonomic functions of CN IX and X: • dysphonia
The carotid reflex is central to blood
pressure homeostasis. CN IX mediates
• deviated uvula
the afferent limb from baroreceptors • abnormal gag reflex
monitoring blood pressure in the • poor cough
carotid bodies and carotid sinus,
whereas many efferent responses are Central
mediated via the vagus. It is difficult
Important central nervous
to detect subtle dysfunction clinically
but the carotid reflex can be assessed system causes include:
by an ECG recording of heart rate • lateral medullary infarc-
(HR): tion
• respiration: HR should vary <10 beats • syrinx
per minute (b.p.m.) at rest
• standing: HR should increase by • tumours
>10 b.p.m. • motor neuron disease
• Valsalva manoeuvre: increase in HR
• carotid massage: decrease in HR Peripheral
• lying and standing blood pressure Important peripheral causes
should differ by no more than
30 mmHg systolic or 15 mmHg
include:
diastolic • tumours (e.g. metastasis
at the jugular foramen)
The neck (CN XI) 73
• aneurysms
• basal meningitis
• peripheral nerve disorders (e.g. Guillain–Barré syndrome)
• glossopharyngeal neuralgia
• mediastinal pathology can involve the vagus nerve
Approach
CN XI is a purely motor nerve that innervates the sternocleido-
mastoid and trapezius muscles. General inspection of the neck
is appropriate at this stage and palpation for lymphadenopathy
should also be performed.
Sequence
Inspect the neck, looking for:
• head drop suggestive of muscle disease/dystrophy
• fasciculations or wasting of sternocleidomastoid or trape-
zius
• any scars or swellings
Following the inspection:
1. ask the patient to shrug their shoulders. Push down on them
to assess strength
2. ask them to turn their head to the right and then attempt to
straighten it. This tests the left sternocleidomastoid muscle.
Repeat for the other side
3. palpate for any lymphadenopathy
74 Head and neck (cranial nerves)
Central
These include:
• medullary infarction
• syrinx
• motor neuron disease
• high cervical injury
Peripheral
These include:
• neck trauma, including surgery
• muscle disorders/dystrophies
• peripheral neuropathies
• motor neuron disease
Lymphadenopathy
This includes the following:
• any cause of cervical lymphadenopathy
• lymph nodes may directly compress the accessory nerve
• lymphadenopathy in the context of neurological dysfunc-
tion may indicate a paraneoplastic syndrome
Upper limbs 4
4.1 Objectives
Examination of the upper limbs aims to further identify any
neurological deficit, localise it and aid in determining the
underlying pathological process.
There is a traditional routine that neurologists follow:
• general inspection
• tone
• power
• reflexes
• co-ordination
• sensation
Think: To (tone) Postpone (power) Reflexes (reflexes)
Constitutes (co-ordination) Sacrilege (sensation).
There are three aims of this stage of the examination:
1. identify any syndrome or obvious abnormalities from
general inspection
2. determine whether there is an upper motor neuron (UMN)
or lower motor neuron (LMN) lesion
3. determine whether the lesion is cortical, spinal, root,
peripheral nerve or muscle
Step 3 is the one at which most get lost, but some sound anatomy
and a systematic examination routine are all that is required.
Table 4.1 Summary of the main upper limb peripheral nerve origins and functions
Anatomy and physiology review 79
C2
C3
C2 C4
C3 C5
C4 T1
C5 T2 T2
T3 T3
T4 T4
T2 T5 T5
T6
T6
T7
T8 T7
T9 T8
T10 T9
C6 T11 T10
T1 T11
T12
T12
L1 L1
L2
L3
C8
S3
C7
innervates the muscle fibre. The UMN is the cell or cells directly
involved in supplying input to the LMN (e.g. the pyramidal cells
in layer V of the motor cortex).
The LMN is the final output structure to the muscle. Thus if
its cell body, nerve root or peripheral nerve is damaged there
80 Upper limbs
Musculocutaneous nerve
Key anatomy of the musculocutaneous nerve:
• roots C5/6
• lateral cord of the brachial plexus
• sensory: lateral cutaneous nerve of the forearm (lateral
forearm from the elbow to the wrist)
• motor: biceps brachii (flexes supinated forearm), brachialis
(synergist to biceps)
Axillary nerve
Key anatomy of the axillary nerve:
• roots C5/6
• posterior cord of the brachial plexus
• sensory: patch on the lateral aspect of the shoulder
• motor: deltoid (abducts the upper arm)
Radial nerve
Key anatomy of the radial nerve:
• divides after the antecubital fossa to give the posterior
interosseous nerve (PIN) and superficial radial nerve
• roots C5–8 (mostly C6/7)
• posterior cord of the brachial plexus
• sensory: posterior cutaneous nerve of the arm (dorsolateral
aspect of the upper arm), posterior cutaneous nerve of the
forearm (dorsolateral surface of the hand)
• motor: extensor muscles of the upper limb. Key muscles
include: triceps (radial; extends forearm, C7), extensor carpi
Anatomy and physiology review 81
Median nerve
Key anatomy of the median nerve:
• anterior interosseous nerve (AIN) branches off after the
antecubital fossa. The palmar sensory branch divides before
the carpal tunnel
• roots C6–T1 (mostly C8/T1)
• lateral and medial cords of the brachial plexus
• sensory: palmar sensory branch – the lateral aspect of the
palm from the lateral half of the base of the ring finger to
the proximal phalanx of the thumb; portion through carpal
tunnel – palmar surface of the first, second and lateral half
of the third fingers, dorsal aspect of the same and the distal
phalanx of the thumb
• motor: all flexors in the forearm except flexor carpi ulnaris
and part of flexor digitorum profundus. Key muscles include:
pronator teres (median; pronates the forearm, C6/7), flexor
carpi radialis (median; flexes and abducts the hand at the wrist,
C6/7), flexor pollicis longus
(AIN; flexes the distal Clinical insight
phalanx of the thumb, C8),
LOAF is a useful mnemonic for the main
flexor digitorum profundus motor functions of the median nerve:
I and II (AIN; flexes the L first and second Lumbricals
distal phalanx of the index O Opponens pollicis
and middle fingers, C8), A Abductor pollicis brevis
F Flexor pollicis longus
abductor pollicis brevis
82 Upper limbs
It is organised so that:
• five roots join to form three trunks (upper, middle,
lower)
• three trunks split/join to form three cords (lateral, posterior,
medial)
• three cords split/join to form the five major peripheral nerves
• In addition to the muscles innervated by the major
peripheral nerves ultimately formed from the trunks and
cords, there are additional smaller nerves that branch off
cords and trunks and aid in localisation
Sensory function
The sensory function in the limbs can be divided into four
modalities:
1. pain (assessed by pin-prick testing (PP))
2. temperature (T°C)
3. joint position sense (JPS)
4. vibration sense (Vib)
Pain and temperature fibres decussate in the spinal cord via the
anterior commissure at the level they enter it and are carried in
the contralateral lateral columns (Figure 4.3). JPS and Vib are
Roots
C5
Trunks C6
Divisions C7
Cords
Nerve C8
Lateral cord T1
Posterior cord
Musculoskeletal Medial
nerve cord
Axillary nerve
Radial nerve
Median nerve
Ulnar nerve
a b c
Posterior cord Anterior Lateral
syndrome cord syndrome cord syndrome
d e f
Central cord lesion
Figure 4.3 Spinal cord anatomy and lesions. (a) Ventral horn: cell bodies of lower
motor neurons. (b) Lateral columns (blue) receive pin-prick (PP) and temperature
(T°C) sensation input from the contralateral body via fibres crossing the midline
through the anterior commissure. (c) Dorsal columns (blue) receive joint position
sense (JPS) and vibration sense (Vib) from the ipsilateral body via fibres that cross
at the medulla. (d) Posterior cord syndrome. Loss of JPS and Vib below the lesion.
(e) Anterior cord syndrome. Loss of PP and T°C sensation and weakness below the
lesion. (f ) Lateral cord syndrome. Loss of ipsilateral JPS and Vib and contralateral
PP and T°C sensation and weakness below the lesion. (g) Central cord lesion.
Disruption of the crossing PP and T°C fibres supplying the lateral columns
Patterns of weakness
These include:
• UMN lesion: typically this produces increased tone, hyper-
reflexia and spastic weakness
• LMN lesion: usually produces reduced tone, low or absent
reflexes and flaccid weakness
• neuromuscular junction: relatively rare, this will give
characteristic fatigable weakness in myasthenia gravis
(i.e. weakness gets worse on repetitive movements) or
facilitation in Lambert–Eaton myasthenic syndrome (i.e.
weakness improves after a few contractions). It tends to
affect highly active muscles, including the extraocular
muscles. Reflexes and sensation are generally normal
86 Upper limbs
Paraesthesia
‘Tingly bits’are a common complaint in the neurologist’s clinic. The
causes range from anxiety or functional disorders to peripheral
nerve, root and spinal cord lesions. They are rarely - despite
patient’s fears – a presentation of central lesions such as tumours.
Patients may describe pins and needles, watery sensations,
sharp sensations, tightness, burning, heaviness, etc. The
distribution is often helpful:
Clinical features and pathophysiology 87
Sensory loss
Careful attention to the pattern and modalities of sensory loss
on examination can greatly aid localisation. Causes of sensory
loss include:
• peripheral nerve/plexus: ‘trapped nerves’ give sensory loss
in the whole nerve distribution below the lesion
• polyneuropathies are
usually length dependent, Clinical insight
meaning that the longer
Severe polyneuropathies can look
nerves (distal sensation) like a spinal cord lesion if the more
are affected first, leading proximal peripheral nerves are affected.
to the classic glove-and- A spinal cord lesion will give a spinal
stocking distribution level where there is complete loss of
• stroke will typically cause affected modalities below the lesion,
whereas even a severe polyneuropathy
sensory loss rather than will usually spare a region of sensation
positive phenomena such in a strip running down the midline of
as pain or paraesthesia the back.
• nerve root: sensory loss This is because the paraspinal cutaneous
nerves are among the shortest nerves
may be in only one or
and last to be affected in a neuropathy.
two modalities at first but Therefore, when a spinal lesion is
is usually associated with clinically suspected always check
radicular pain sensation down the spine itself to
• dorsal column: lesions exclude a severe length-dependent
polyneuropathy.
here cause a loss of JPS
88 Upper limbs
Approach
The patient undresses to their underwear to enable full
assessment of their muscles and nerves. Instruct women to
keep their bra on.
Sequence
In generally assessing the upper limb, observe from in front
and then behind. Look for:
1. asymmetry in posture of the upper limbs, e.g. contracted
spastic hemiplegia
2. muscle wasting, particularly the first dorsal interosseous
and the thenar and hypothenar eminences
3. fasciculations: these may be evident only after prolonged
observation
4. pronator drift: ask the patient to ‘put your hands out in front
of you, palms up, and close your eyes’
4.5 Tone
Objective
The purpose of this part of the examination is to identify any
pathologically increased or decreased tone.
Sequence
To assess the tone of the upper limb:
1. take the patients hand as though to shake it
2. tell them ‘let me take the weight of your arm’
3. flex and extend and rotate the arm at the wrist, elbow and
shoulder at variable speed
4. ask the patient to ‘open and close your other fist’ to
accentuate any increased tone
4.6 Power
Objective
This stage is used to examine the strength of individual muscles
and thereby indirectly peripheral nerve, brachial plexus, nerve
root and CNS function.
Approach
The patient is asked to move their arms into various positions
and then the examiner attempts to overcome their strength.
Table 4.2 shows how muscle strength is graded.
Sequence
The sequence tests the muscles in turn in a logical order to
assess a number of muscles from each major peripheral nerve
and nerve root. The verbal instructions are given in Table 4.3, as
is the muscle being tested, the innervating nerve, the supplying
brachial plexus cord and the major root. Figures 4.4–4.7
demonstrate a useful order in which to test the key muscles.
Note that there is some variation in nerve root and plexus
contributions to peripheral nerves.
Grade Description
0 No movement
1 Perceptible flicker of muscle contraction
2 Movement only if gravity eliminated
3 Can overcome gravity but not resistance
4 Can be overcome by examiner
5 Normal strength
Table 4.2 Medical Resarch Council (MRC) power grade. Sometimes grade 4 is
designated 4+ when there is considerable but not full strength, and designated
4– when easily overpowered.
Instruction Muscle Muscle action Nerve Plexus cord Root
Lift your elbows up and out Deltoid Shoulder abduction Ax P C5/6
Make arms like a boxer Biceps brachii Elbow flexion MS L C5/6
Make arms like a boxer Triceps Elbow extension R P C7
Make fists and cock your wrists back Extensor carpi radialis longus Wrist extension and abduction R P C6
Make fists and cock your wrists back Extensor carpi ulnaris Wrist extension and adduction R P C7
Keep your fingers out straight Extensor digitorum Finger extension R P C7
Stick your thumbs out to the side Extensor pollicis brevis Thumb abduction R P C7
Grip my finger tips Flexor digitorum profundus Flexion of distal phalanx Md L, Ml C8
I and II
Bend your thumbs Flexor pollicis longus Flexion of thumb Md L, Ml C8
Touch your thumbs to the base of your Opponens pollicis Thumb opposition Md L, Ml T1
little finger
Spread your fingers wide Flexor carpi ulnaris Finger abduction U Ml C8
Spread your fingers wide 1st dorsal interosseous Finger abduction U Ml T1
Keep your fingers together 2nd palmar interosseous Finger adduction U Ml T1
Keep your thumb on your palm Adductor pollicis Thumb adduction U Ml T1
Power
Table 4.3 Sequence of instructions for examining power in the upper limbs. Ax, axillary nerve. L, lateral. Md, median nerve. Ml, medial. MS,
musculoskeletal nerve. P, posterior. R, radial nerve. U, ulnar nerve.
91
92 Upper limbs
Flaccid weakness
Flaccid weakness can be caused by:
• myopathy: proximal weakness is classic for most muscle
diseases. An exception is inclusion body myositis, which
Power 93
a b
c d
Spastic weakness
The causes of spastic weakness are:
Power 95
a b
c d
Figure 4.7 Assessment of the power of the ulnar nerve. (a) Flexor carpi ulnaris,
C8, ulnar. (b) First dorsal interosseous, T1, ulnar. (c) Second palmar interosseous,
T1, ulnar. (d) Adductor pollicis, T1, ulnar
Table 4.4 Summary of key clinical and laboratory features of myasthenia gravis
(MG) and Lambert–Eaton myasthenic syndrome (LEMS). CMAP, compound
muscle action potential.
4.7 Reflexes
Objective
This part of the examination is used to elicit reflexes and
determine whether they are absent, reduced, normal or
increased (hyper-reflexic).
Approach
Various muscle tendons are tapped to test their reflexes. The
patient is positioned with their hands on their lap so that the
upper limb muscles are relaxed and elbows slightly bent.
Reflexes 97
Equipment
Reflex testing requires a tendon hammer.
Sequence
Tricep, bicep and supinator reflexes should be tested:
1. tap the tendon of triceps on each arm (C7)
2. tap the tendon of biceps on each arm (C6)
3. tap the tendon of supinator on each arm (C5)
4. if any reflex cannot be elicited, ask the patient to clench their
teeth tight and then retest the reflex (reinforcement).
4.8 Co-ordination
Sequence
To assess co-ordination in the upper limb:
1. ask the patient to ‘Touch your nose with your right index finger’
2. ask them to ‘Touch my finger with yours’ while holding your
finger at a distance forcing them to fully extend their arm
Sensation 99
4.9 Sensation
Objective
The purpose of this part of the examination is to assess the
sensory function of the peripheral nerves, nerve roots and
spinal cord supplying the upper limbs.
Approach
The patient has their sensation tested with their outer garments
removed. Inform the patient that you are going to test their
sense of touch in a number of ways, including with a dull pin
tip that will not break their skin. Tell them that you are going
to ask them whether the PP is sharp or dull and to compare it
between sides.
The principles of the sensory examination are to:
• start distally and work proximally
100 Upper limbs
Equipment
This requires a Neurotip, tuning fork and universal containers
with hot and cold water.
Sequence
Test the function of the lateral and dorsal columns in turn
Lateral columns
These are tested with either PP (pain) or hot and cold water (T°C):
1. touch the patient’s sternum or forehead with the tip of the
Neurotip to show the patient what it feels like
2. touch each of the following areas and ask ‘Does it feel sharp
or dull?’:
• dorsum of the hand in the area of the radial nerve (radial;
C6)
• medial aspect of the middle finger (median; C7)
• medial aspect of the little finger (ulnar; C8)
3. then touch it to each of the remaining dermatomes:
• medial surface of the forearm (T1)
• lateral surface of the forearm (C6)
• medial surface of the arm (T2)
• lateral aspect of the shoulder (axillary; C5)
4. repeat on the other side
5. if there are any abnormalities, repeat on the other side asking
the patient to tell you if it feels the same on both sides
6. if there are any abnormalities, move in a proximal direction
and retest until sensation returns to normal
7. in place of PP you can use hot and cold water in universal
containers, touching the skin in the above sequence, asking
if it is hot or cold
Dorsal columns
These are tested with a tuning fork (vibration) or joint
movement (JPS).
Sensation 101
Vibration
To examine vibration sense:
1. tap the tuning fork
2. place on the patient’s clavicle and tell the patient ‘This is
what it feels like, can you feel it buzzing?’
3. tap before each placement
4. place the tuning fork on:
• distal phalanx of the thumb (radial; C6)
• distal phalanx of the middle finger (median; C7)
• distal phalanx of the little finger (ulnar; C8)
5. then test the remainder of the major dermatomes:
• medial epicondyle of the elbow (T1)
• lateral epicondyle of the elbow (C6)
• bony head of the humerus (C5)
• sternal edges (T2)
6. repeat on other side
7. If there are any abnormalities, repeat on the other side asking
the patient to tell you if it feels the same on both sides
8. If there are any abnormalities, move in a proximal direction
and retest until sensation returns to normal
Proprioception
Alternatively, In place of vibration you can test proprioception
by moving joints:
1. isolate the joint by placing fingers proximally and distally
2. ask the patient to close their eyes and tell you if the joint
moves up or down
3. move the joint up or down - normally even tiny movements
are appreciated
4. take care to place fingers to the sides of the joints rather than
on top as you will otherwise stimulate pressure receptors
rather than joint position sense
5. start at the distal joints and move proximally until there is
normal perception of movement
Table 4.7 Summary of clinical features of spinal cord syndromes. JPS, joint
position sense.
System summary 103
Lower limbs 5
5.1 Objectives
Examination of the lower limbs is very similar in approach to that
of the upper limbs. The same sequence of examining tone, power,
reflexes, co-ordination and sensation is followed and the same
general rules about upper motor neuron (UMN) and lower motor
neuron (LMN) lesions and patterns of spinal cord injury apply.
Table 5.1 Summary of the major motor functions of the peripheral nerves in
the lower limbs
Gluteal nerve
Key anatomy of the gluteal nerve:
• The superior gluteal nerve supplies gluteus medius (GluMe)
and minimus (GluMi); the inferior gluteal nerve supplies
gluteus maximus (GluMax)
• roots L4/5
• sensory: none
• motor: GluMax is a powerful hip extensor; GluMe and GluMi
internally rotate and abduct the thigh
Anatomy and physiology review 107
Obturator nerve
Key anatomy of the obturator nerve:
• roots: L2/3
• sensory: supplies sensation to the medial aspect of the thigh
• motor: adductors of the lower limb
Sciatic nerve
Key anatomical features of the proximal portion (from the
origin to the division of the tibial and common peroneal nerves):
• roots: L5/S1/S2
• sensory: the posterior cutaneous nerve of the thigh
originates at the same level as, and travels close by, the
sciatic nerve. It supplies the posterior aspect of the thigh
• motor: the ‘hamstrings’ flex the knee
Common peroneal
The common peroneal nerve gives rise to the superficial and
deep peroneal nerves at the head of the fibula. Key anatomical
features include:
• roots: L4/L5/S1
108 Lower limbs
Tibial
Key anatomical features of the tibial nerve:
• roots: L4–S2
• sensory: the sural nerve and the plantar nerves supply the
lateral aspect and the sole of the foot, respectively
• motor: gastrocnemius plantarflexes the foot; tibialis
posterior inverts the foot;
flexor digitorum and hallucis
Clinical insight longus flex the toes; the small
Common peroneal neuropathy: muscles of the foot ‘cup’ the
• foot drop, weak foot eversion but toes
spared inversion
• sensory loss over the dorsum of the
foot and anterior and lateral aspects The lumbosacral plexus
of the leg The lumbosacral plexus is
• causes include trauma at the head of the lower limb equivalent
the fibula, chronic crossing of legs,
prolonged squatting, knee trauma
of the brachial plexus. The
anatomy is more complex
than in the brachial plexus
and a working knowledge
Clinical insight of it is a specialist area.
Retroperitoneal tumours can
Tibial neuropathy:
cause compressive lesions, as
• weakness of plantarflexion
• loss of sensation on the sole of the foot can local nerve infarction or
• causes: trauma or surgery in the inflammation.
popliteal fossa or ankle, entrapment
at the posterior tarsal tunnel (pain Intervertebral discs
and numbness at the ankle and sole),
diabetes Key anatomy of intervertebral
discs:
Clinical features and pathophysiology 109
Table 5.2 Relation between the prolapsed disc level, exiting nerve root at that
level, and the root compressed by the prolapse
Approach
Ask the patient to remove their outer garments.
Sequence
In generally assessing the lower limb, observe from in front and
then behind. Look for:
1. asymmetry in posture of the lower limbs
2. muscle wasting, particularly tibialis anterior and the
quadriceps
3. foot deformities such as pes cavus
4. fasciculations: these may be evident only after prolonged
observation
5.5 Tone
Objective
The aim of this part of the examination is to identify any
pathologically increased or decreased tone.
Sequence
To examine tone:
1. ask the patient to lie flat on the couch
2. roll their legs at the thigh, watching the ankle
3. pull up sharply behind the knee, dragging the heel up the
couch
4. normally, the foot will wiggle quite freely at the ankle when
you roll the thighs and the ankle will drag up the surface of
the couch when the knee is jerked up.
5.6 Power
Objective
This part of the assessment examines the strength of individual
muscles, thereby assessing muscle function and indirectly
peripheral nerve, nerve root, spinal cord and cortical function.
Power 113
Approach
The general principles of assessing power in the upper limbs
(Chapter 4) apply here too. The aim is to grade the muscle
strength (see Table 4.2).
Sequence
The sequence tests the muscles in turn in a logical order to assess
a number of muscles from each major peripheral nerve and
nerve root. The verbal instructions are given in Table 5.3, as is the
muscle being tested, the innervating nerve and the major root.
Figures 5.1–5.4 demonstrate the key muscles to test. There is
some variation in nerve root contributions to peripheral nerves.
LMN lesion
The differential diagnosis is fairly wide and is between muscle,
mononeuropathy, polyneuropathy, plexus and root. The
following may help differentiate them:
• myopathy. This will give the following:
– LMN signs
– proximal weakness with difficulty standing or squatting
– usually symmetrical
– often also tender muscles
114
Don’t let me separate your legs Adductors Adduction at the hip Obturator L2/3
Bend your knee, don’t let me turn your Gluteus medius and minimus Internal rotation of the Superior gluteal L4/5
leg out thigh
Bend your knee, don’t let me bend it Quadriceps Extension at the knee Femoral L3/4
more
Bend your knee, don’t let me straighten Hamstrings Flexion at the knee Sciatic S1
it
Push your foot down Gastrocnemius Plantarflexion at the ankle Tibial S1/2
Turn your foot in Tibialis posterior Inversion of the foot Tibial L4/5
Curl your toes Small muscles of the foot Cupping of the foot Tibial S1/2
Point your foot towards your head Tibialis anterior Dorsiflexion at the ankle Deep peroneal L4
Point your big toe towards your head Extensor hallucis longus Extension of the toe Deep peroneal L5
Turn your foot out Peroneus longus and brevis Eversion of the foot Superficial peroneal L5/S1
Table 5.3 For each instruction ask the patient to position their limb as described and tell them ‘Don’t let me move it’ before applying an antagonistic
force
Power 115
a b
a b
a b
a b
c
Reflexes 117
• mononeuropathies show
weakness in a pattern
Clinical insight
attributable to a single The hallmark of nerve root disease is
the progression from radicular pain,
nerve
through radicular sensory loss to
• polyneuropathies show radicular weakness. Radicular pain is
weakness in muscles inner usually the first symptom of nerve root
vated by several peripheral compression. The radiation of the pain
nerves. Typically, distal is usually indicates the level of origin:
worse than proximal and it Nerve Pain radiation
is usually symmetrical root
• sacral plexopathies are affected
C5 Shoulder
essentially unilateral C6 Lateral forearm and thumb
polyneuropathies with C7 Dorsum of hand and
muscles affected from middle finger
multiple nerves C8 Medial forearm, medial two
fingers
• a root lesion is most readily L1 Groin
identified by the distribution L2 Medial thigh
of pain; however, if there is L3 Knee
L4 Inner calf
involvement of the ventral L5 Outer calf and great toe
or spinal root, weakness will S1 Lateral foot and sole
also be seen. This will be in S2 Posterior thigh
muscles not restricted to a
single peripheral nerve but
to a recognisable spinal Clinical insight
level Getting above the lesion: when signs
of weakness (or sensory disturbance) are
What happens next? found in the arms or legs a helpful strategy
Move on to test the reflexes. is to attempt to ‘get above the lesion’. This
means finding the level of the nervous
system above which function is normal.
5.7 Reflexes Since lesions in the central nervous system
or peripheral nervous system will cause
Objective weakness or sensory disturbance distally,
The aim of this part of the the level at which power returns to normal
examination is to elicit indicates that the lesion is below this.
reflexes and determine
whether they are absent, reduced, normal or increased (hyper-
reflexic).
118 Lower limbs
Approach
During the examination, various muscle tendons are tapped
to test their reflexes.
Equipment
A tendon hammer is required.
Sequence
To assess lower limb reflexes and clonus:
1. ask the patient to lie flat on the couch
2. take the weight of each leg in turn by lifting under the knee
3. tap the patellar tendon for the knee jerk (L3/4)
4. with legs flat tap the medial aspect of the knee where the
adductors attach; watch both legs for adduction: crossed
adductor reflex (L2–5)
5. flex the knee slightly, turn the foot outward and hold it
dorsiflexed, tap the Achilles tendon: the ankle jerk (S1/2)
6. stroke the lateral sole of the foot upwards and across to the
ball of the foot, observing the initial direction of movement
of the great toe: the plantar reflex
7. check for clonus by:
• gently rolling the ankle briefly then forcefully holding it
dorsiflexed
• observe any rhythmic plantarflexion of the ankle
• more than four beats is likely to be pathological
8. if any reflex cannot be elicited, ask the patient to grip
their hands together and pull hard (reinforcement) as you
test
5.8 Co-ordination
Objective
The next step is to assess the co-ordination of the lower
limbs.
Sequence
Ask the patient to:
1. ‘lift your heel off the couch’
2. ‘touch it to your other knee’
3. ‘run it down your shin’
4. ‘lift it up and do it again’
5. ‘tap out a rhythm with your heel’
5.9 Sensation
Objective
The purpose of the final step in this part of the examination is
to assess the sensory function of the peripheral nerves, nerve
roots and spinal cord supplying the lower limbs. See Figure 5.5
for the dermatomes of the lower limbs.
Approach
The patient has their sensation tested with their outer
garments removed. Women should keep their bra on. Inform
the patient that you are going to test their sense of touch in
a number of ways, including with a dull pin tip that will not
break their skin. Tell them that you are going to ask them
whether the pin-prick is sharp or dull and to compare it
between sides.
The principles of the sensory examination are to:
• start distally and work proximally
• test each major peripheral nerve
• test each major dermatome
• test both lateral and dorsal columns of the spinal cord
• map out any area of sensory change encountered
Equipment
This requires a Neurotip, tuning fork and universal containers
with hot and cold water.
Sequence
Test the function of the lateral and dorsal columns in turn.
Lateral columns
These are tested with either pin-prick (PP) (pain) or hot and
cold water (temperature (T°C)):
1. touch the patient’s sternum or forehead with the tip of the
Neurotip to show the patient what it feels like
2. touch each of the following areas and ask ‘Does it feel sharp
or dull?’:
• lateral aspect of the last toe (sural nerve; S1)
• dorsal aspect of the great toe (superficial peroneal nerve;
L5)
• web space between the great toe and second toe (deep
peroneal nerve; L5)
• medial aspect of the tibia (saphenous nerve; L4)
• anterior aspect of the knee (femoral nerve; L3)
• lateral aspect of the thigh (lateral cutaneous nerve of
the thigh; L2)
• popliteal fossa (posterior cutaneous nerve of the thigh; S2)
3. this is usually sufficient to screen in a general examination.
However, if cauda equina syndrome is suspected, also ensure
to check perianal and perineal sensation:
122 Lower limbs
Dorsal columns
These are tested with a tuning fork (vibration) or joint
movement (JPS):
Vibration
To examine vibration sense:
1. tap the tuning fork
2. place on the patient’s clavicle, or forehead if a high thoracic
lesion is possible, and tell the patient ‘This is what it feels like,
can you feel it buzzing?’
3. tap before each placement
4. place the tuning fork on:
• lateral maleolus (sural nerve; S1)
• distal interphalangeal joint of the great toe (superficial
peroneal nerve; L5)
• mid-tibia (saphenous nerve; L4)
• tibial plateau (femoral nerve; L3)
• hip (L1)
5. if there is an area of abnormal sensation that persists up
to L1, higher dermatomes must be tested until an area of
Sensation 123
Cerebellum 6
6.1 Objectives
The gross motor functions of the cerebellum are tested dur-
ing several other stages of the neurological examination, e.g.
in looking for nystagmus in the cranial nerve examination or
testing co-ordination in the limb examination. Nonetheless,
a systematic approach to examining cerebellar function is
needed when the history or initial examination indicates
cerebellar disease.
Fastigial nucleus
Interposed nucleus
Dentate nucleus
Flocculondular
lobe Vestibular inputs
and outputs
Figure 6.1 The structural and functional inputs and outputs of the cerebellum
Vertigo
This is the sensation of the environment spinning while
stationary – like ‘stepping off a roundabout’. Patients may not
be familiar with this meaning of the word, and so care should
be taken to fully determine the nature of any dizziness, faintness
or unsteadiness that they report.
Ataxia
Ataxia is objective dysfunction of balance. Ataxia is truncal
when it affects the posture of the trunk. This is evident even
while sitting upright. Appendicular ataxia is when a limb is
affected. Ataxia may be evident on walking, when a patient will
tend to fall to the affected side of a unilateral lesion.
Nystagmus
Nystagmus is the inability to maintain gaze fixation. There is a
slow phase of eye movement away from the target followed
by a rapid saccade to correct it. The direction of the fast phase
is the direction of nystagmus (i.e. if the slow phase is to the left
then the fast correction is back to the right and it is described
as right-beating nystagmus).
Nystagmus may be normal (physiological) or abnormal from
peripheral lesions (i.e. to the
vestibular system) or central Clinical insight
lesions. It can occur at rest; be
Peripheral nystagmus tends to be
gaze evoked; or be position unilateral (i.e. it occurs mainly when
evoked. Central lesions (e.g. looking in one direction) with the fast
in the cerebellum) tend phase pointing away from the lesion.
to produce spontaneous In central nystagmus, the fast phase
tends to change so that it occurs in the
nystagmus at rest, whereas direction of gaze.
peripheral lesions tend to be
128 Cerebellum
Intention tremor
This is a tremor that increases as the limb approaches the
target. Similar symptoms such as dysmetria (overshooting or
undershooting a target) and impaired check (failure to stop
a limb movement appropriately) also commonly occur in
cerebellar lesions.
Speech disturbance
Typically, cerebellar lesions result in a dysarthria with intact
semantics. There may also be scanning speech in which there
are pauses between words or syllables.
Hypotonia
Decreased tone can occur in acute cerebellar lesions.
Dysdiodochokinesia
This is the inability to accurately perform rapidly alternating
movements. As with many of the clinical abnormalities of
cerebellar disease, it is thought to be due to poor co-ordination
of agonist and antagonist muscles.
Approach
The patient should undress to their under garments.
Sequence
In generally assessing cerebellar function:
1. observe the patient from in front and then behind
2. look for foot deformities, hypothyroid facies or evidence of
chronic liver disease
VANISHD 129
6.5 VANISHD
Objective
The purpose is to systematically review the major clinical
abnormalities found in cerebellar disease: Vertigo, Ataxia,
Nystagmus, Intention tremor, Speech disturbance, Hypotonia
and Dysdiodokokinesia.
Approach
Tell the patient that their ability to perform a range of
movements will be assessed.
Sequence
Assess the patient for features of cerebellar dysfunction using
the acronym VANISHD as a guide
Vertigo
Vertigo is a symptom and therefore should have been clarified
in the history.
130 Cerebellum
Ataxia
To assess for ataxia:
1. ask the patient to sit upright in the chair with their back
forward from the chair back
2. note any oscillations in the trunk, neck or head
3. ask them to stand. Note the position of their feet (i.e. any
broad-based stance)
4. ask them to walk to the end of the room, turn and come
back
5. note the pattern of the gait and whether they fall to one side
Nystagmus
Closely check for nystagmus:
1. ask them to sit again
2. ask them to look at your nose. Note any nystagmus in
primary gaze
3. test their range of eye movements again, noting the
presence and fast-phase direction of any nystagmus
Intention tremor
An intention tremor should have been detected as part of the
examination of the limbs but can be retested here:
1. ask them to touch their nose with their forefinger, and then
to touch your finger; ensure that the patient has to fully
stretch their arm out to reach the target
2. test both sides
3. note whether they miss the target and whether a tremor
emerges as their finger approaches the target
4. also test for impaired check by (1) asking the patient to
hold their arms up like a boxer and to resist your pull;
(2) pull against their biceps; (3) release suddenly, noting if
their flexed arm pulls back in an exaggerated manner
Speech
Speech is usually evident from the initial examination, but ask
them (1) to describe the room, looking for dysarthria or scan-
ning speech and (2) to say ‘Ah’, ‘Gah’, ‘But’
VANISHD 131
Hypotonia
Take the patient’s arms and legs in turn and check for tone if
not already assessed
Dysdiodochokinesia
Dysdiodochokinesia can be demonstrated:
1. ask the patient to clap one hand on top of the other, turning
it from front to back each time
2. demonstrate this for them
3. note any slowed or poorly co-ordinated efforts
4. check their heel–shin co-ordination as described in
Chapter 5
Table 6.1 Cerebellar syndromes. Lesions of the vermis tend to cause more
truncal ataxia than limb ataxia, and fewer obvious limb signs. Lesions in the
hemispheres cause a greater range of symptoms and include prominent limb
signs ipsilateral to the lesion
132 Cerebellum
Developmental or hereditary
Key causes include Arnold–Chiari and Dandy–Walker malforma-
tions and the hereditary ataxias.
Arnold–Chiari malformation This is often asymptomatic or can
present with headaches or nystagmus.
Dandy–Walker malformation This may present with hydro-
cephalus or delayed development in childhood. Other features
such as nystagmus commonly occur.
The hereditary ataxias These include a large number of rare
autosomal dominant and recessive conditions:
• the most common autosomal dominant conditions are the
spinocerebellar ataxias, which are chronic, progressive
conditions. There is usually a family history and genetic
testing for mutations (which are usually CAG trinucleotide
repeats) is available
• the most common autosomal recessive condition is
Friedreich’s ataxia. This is a chronic, progressive disease
with onset between infancy and the twenties. There is often
areflexia of the ankles, cardiomyopathy and diabetes in up
to one-quarter of cases
Acquired There are a wide range of acquired causes of
cerebellar disease, including vascular, toxic, neoplastic, infective
and autoimmune pathologies.
Vascular Posterior circulation syndrome ischaemic strokes
commonly cause cerebellar signs:
• the posterior inferior cerebellar artery is the most commonly
affected and infarction in this territory causes sudden
onset vertigo, nystagmus, dysarthria, Horner’s syndrome
(ipsilateral), facial sensory loss (ipsilateral), trunk and limb
sensory loss (contralateral) and limb ataxia (ipsilateral)
VANISHD 133
Higher 7
cortical function
7.1 Objectives
Examination of higher cortical function is an important
component of the neurological assessment. Although it is less
useful for fine localisation, it is very helpful in determining the
impact of a disease process on a patient’s cognitive processes
and for assessing its progression over time. Two commonly
used bedside tests of cognition are the Mini-Mental State
Examination (MMSE) and the Revised Addenbrooke’s
Cognitive Examination (ACE-R). These test the five basic
cognitive domains, which are discussed below.
Language
Language is such a defining feature of our human nature that
the complexity of neural computations that it requires is easily
overlooked. Indeed, language is perhaps the most complex
function of the most complex structure in the universe. In
recent years a ‘dual stream model’ of language processing has
Anatomy and physiology review 137
Memory
There are many types of memory. It is helpful to distinguish
between short-term memory (or working memory) and long-
Figure 7.1 The dual stream model of language function. There is a bilateral
ventral stream underlying speech recognition and a dorsal stream involved with
speech production. BA, Broca’s area; WA, Wernicke’s area; PMcx, premotor cortex;
Acx, auditory cortex; ATL, anterior temporal lobe; ITL, inferior temporal lobe
138 Higher cortical function
Executive function
This term refers to some of the ‘higher’ cortical functions such as
abstraction, inhibition, planning and other social behaviours.
The frontal lobes and basal ganglia appear crucial for such
tasks.
Language
Because of the complexity of language and the multitude of
brain regions underlying its various aspects, it is possible to
Clinical features and pathophysiology 139
Comprehension
Language comprehension
appears to be bilaterally
Clinical insight
localised along the superior Wernicke’s aphasia: damage to
Wernicke’s area in the superior temporal
temporal gyrus. Deficits in gyrus can cause a type of aphasia
language comprehension are known as Wernicke’s or receptive
particularly socially isolating. aphasia. The patient appears unable
Receptive aphasia is to understand language (i.e. cannot
the inability to understand follow instructions), but is easily able to
generate words and sentences even if
language and is also known these are grammatically and semantically
as Wernicke’s aphasia or meaningless.
posterior aphasia.
Reading
Dyslexia is a developmental reading disorder which is usually
evident in early childhood. Alexia refers to the acquired inability
to read in someone previously able to. It is often found along
with dysphasias and is associated with frontal and parietal
lesions.
Writing
An inability to write is called agraphia. This is usually seen in
dominant parietal lobe lesions.
Speech
Deficits in speech include:
• dysphonia: patients with parkinsonism often display a slow,
monotonous and quiet speech
• dysarthria: this is a deficit in speech articulation. There is
no deficit in speech content. It may be caused by a lesion
in the motor cortex, internal capsule, brainstem, cerebellum
or cranial nerves
• dysphasia: receptive dysphasia is the inability to understand
speech; expressive dysphasia is also known as Broca’s or
anterior aphasia and is impairment of the ability to generate
140 Higher cortical function
Memory
The lateral temporal lobes are crucial sites for semantic memory
processes. Memory can appear falsely impaired owing to poor
concentration in depressive states. Alzheimer’s disease, dementia
with Lewy bodies and frontal–temporal dementia all exhibit
profound memory deficits. Progressive supranuclear palsy is
typically associated with well preserved memory function, and
can thereby be distinguished from other neurodegenerative
processes.
Executive function
Deficits in executive functioning often cause substantial
impairment in an individual’s ability to work and to participate
normally in social activities. Deficits in this domain may not be
apparent on initial discussion or history taking. Basic tests of
executive function examine:
• initiation
• abstraction
• set-shifting
Executive functioning tends to be affected in most degenerative
cognitive processes. In many ways it defines a dementing
process; however, it may be quite well preserved in mild
cognitive impairment.
Approach
Firstly, ask the patient whether they are naturally left or right
handed. Then tell the patient that you are going to test their
memory and speech with some very simple questions that will
get a bit more difficult.
Equipment
This stage of the examination requires paper, pen, a photograph
and a newspaper.
Sequence
Examine cognitive function by domain:
• orientation
• attention
• language
• visuoperceptual function and calculation
• memory
• executive function
• cortical release signs (primitive reflexes)
Orientation
Ask the patient the:
• time (hour, day of week, month, year)
• place (ward, building, town, country)
• person (their name, age and date of birth)
Attention
Test attention by asking the patient to:
• recite the months of the
Clinical insight year backwards
When testing a patient’s ability to repeat
• spell WORLD backwards
a span of digits, remember to write • repeat back 7–9 sequen-
down the numbers for yourself to check tially longer numbers (a
whether they are right! test of digit span memory)
Bedside testing of cognitive domains 143
Language
Assess language function for:
• lack of comprehension (receptive dysphasia)
• poor articulation (dysarthria)
• problems expressing or word finding (expressive dysphasia)
To assess language, test the patient’s abilities of:
• conversation: note the length, word choice, articulation and
fluency of speech during the consultation
• language function: asking the patient to describe the
picture in Figure 7.2
• comprehension: ask them the following: ‘What colour are
daffodils?’ (yellow); ‘What do we call a small seat without a
back? (stool); and ‘Close your eyes and stick out your tongue’
• naming: ask them to name a few objects close to hand (e.g.
pen, belt, cup)
• repetition: ask them to repeat: ‘baby’; ‘hippopotamus’;
‘education’; a name and address (e.g. ‘Peter Godfrey, 14
Woodbean Avenue, Durham’) and tell them to try to remember
it
• writing: ask them to write a short, sensible, sentence
Memory
To test the patient’s memory, ask them:
• to recall the name and address from earlier
• to describe the picture you showed them
• ‘who is the Prime Minister?’; ‘what were the dates of the
Second World War?’; and ‘who was the US President who
was assassinated in 1963?’
• to name a few famous people shown in a newspaper
Executive function
Proverbs Have them explain the following proverbs:
• ‘strike while the iron is hot’
• ‘the apple never falls far from the tree’
• ‘it is always darkest before the dawn’
Fluency Have them name as many words as possible that begin
with the letter C in 60 seconds.
Alzheimer’s disease
This has slow onset and gradual progression of memory loss
with impairment in other cognitive domains with time. Often,
patients have language problems, apraxias or executive
dysfunction.
Vascular dementia
There is often executive dysfunction initially. There is also a
characteristic stepwise pattern of abrupt declines in cognitive
function in the presence of cerebrovascular disease.
Bedside testing of cognitive domains 147
Frontotemporal dementia
This can be either behavioural dominant or language dominant:
• behavioural-dominant patients show changes in personality
and executive function
• language-dominant patients show expressive dysphasia
Both show memory impairment and characteristic preservation
of visuospatial function.
148 Higher cortical function
Corticobasal degeneration
Patients have cognitive dysfunction together with signs
and symptoms of corticobasal degeneration, including
asymmetrical rigidity. Cognitive impairment typically includes
limb apraxia and neglect.
Autonomic 8
nervous system
The autonomic nervous system (ANS) comprises the
sympathetic and parasympathetic divisions in a diffuse
network of central and peripheral connections that mediate
homeostatic control of much of the body’s ‘vegetative functions’.
The sympathetic and parasympathetic divisions generally act
antagonistically to allow fine control over functions such as
heart rate, blood pressure, respiration and a host of other core
physiological functions.
8.1 Objectives
Both central nervous system (CNS) and peripheral nervous
system lesions can affect the ANS. Often, the dysfunction
is subtle and difficult to detect clinically owing to the large
moment-to-moment and interindividual variation in many of
the affected physiological parameters. However, it is essential
to be aware of some simple bedside tests that can help in
assessing the ANS.
The process explained in this chapter does not need to be
carried out routinely in every patient; rather, it is required only
in those with known neurological disease likely to involve the
ANS or in those with relevant symptoms or signs from the
history and remainder of the examination.
Parasympathetic Sympathetic
Constricts
pupil
Stimulates
salivary C1 Reduces salivary
galand
C2 gland secretions
C3
C4 Superior
C5 Cervical
CN X Middle
C6 ganglia
C7 Inferior
Decreases heart rate C8
And contractility T1 Increase heart rate
T2 and contractility
Constricts bronchi T3 Dilates bronchi
smooth muscle T4 smooth muscle
T5
Decreases peristalsis
Increases peristalsis and T6
and gastric secretions
T7
gastric secretions
T8 Stimulates
T9 gluconeogenesis
Increases bile secretions T10
T11 Stimulates release of
T12 adrenaline and
L1 noradrenaline
L2
L3 Relaxes bladder
L4
L5 Sympathetic chain
S1
S2
Contracts S3
bladder S4
S5
Dorsal root
Pre- ganglionic
sympathetic neuron
Motor neuron Dorsal root ganglia
Ventral root
Post- ganglionic
sympathetic neuron
Sympathetic chain
Spinal nerve
Grey communicating
ramus
White communicating
ramus
Peripheral nerve
Sympathetic chain
ganglion
8.4 History
Objective
The objective of the history is to elicit specific details relevant to
autonomic dysfunction. These may have been missed because
the patient fails to think they are significant or the doctor does
not think to ask.
Approach
Tell the patient that you need to ask some questions relating
to how the brain and nerves control some bodily functions.
Sequence
Work through the major functions of the ANS, checking for
important symptoms of dysfunction. Key questions are:
1. ‘any faint spells? What about on standing/coughing/
straining/eating?’
2. ‘any changes to your skin?’
3. ‘do you get hot or sweaty flushes?’
4. ‘any change in your bladder function? Any incontinence?
Are you finding it more difficult to pass urine?’
5. ‘are your bowels moving normally?’
Bedside examination and tests 157
Approach
Tell the patient you need to monitor their heart rate and blood
pressure while they perform a few minor acts including lying,
standing, straining and squeezing a ball.
Equipment
This requires an ECG machine, BP cuff and extra sphygmo
manometer, and a pen torch.
Sequence
Follow the sequence:
1. look at the skin
2. feel the skin (temperature, oedema, etc.)
3. examine the pupils
4. attach the ECG machine and record the following: (a)
lying pulse and BP; (b) standing pulse (initially and at 2–3
minutes) and BP (at 2–3 minutes); (c) heart rate variability
during deep breathing (compare shortest and longest RR
interval over 10 deep breaths); and (d) heart rate variability
during Valsalva
5. ask the patient to squeeze the spare sphygmomanometer
continuously and measure the BP at 2 minutes
158 Autonomic nervous system
Examining the 9
stroke patient
Every junior doctor should be competent in the recognition,
initial assessment and management of acute stroke. It is a
common and serious condition that requires immediate
management decision-making.
Despite the need for a speedy assessment, the history
remains crucial and must be carried out properly and ap-
propriate collateral history sought where needed. Most hos-
pitals now have an acute stroke service and they should be
contacted early for discussion of appropriate investigations
and management.
9.1 Objectives
Assessing the patient with acute onset of focal neurological
symptoms requires a balance between speed and thorough-
ness to ensure:
• symptoms and signs are confirmed
• stroke risk factors are identified
• the lesion is broadly localised
• suitability for thrombolysis is established
Syndrome Features
Total anterior circulation All of:
syndrome Motor or sensory deficit*
Hemianopia
Higher cortical dysfunction
Partial anterior circulation Two of:
syndrome Motor or sensory deficit
Hemianopia
Higher cortical dysfunction
Lacunar syndrome One of:
Pure motor deficit*
Pure sensory deficit*
Sensorimotor deficit*
Ataxic hemiparesis
Without any of:
Higher cortical dysfunction
Posterior circulation syndrome symptoms
Posterior circulation Any of:
syndrome Isolated homonymous hemianopia
Bilateral motor or sensory deficit
Brainstem signs
Cerebellar signs
Table 9.1 The Oxford stroke classification system. *Affecting face, arm and leg.
Clinical features and pathophysiology 163
Anterior circulation
Anterior cerebral
Posterior circulation
Middle cerebral
Posterior
cerebral
Internal carotid
Posterior
communicating
Cerebellar
Basilar
Vertebrals
Figure 9.1 The anterior and posterior circulations refer to the circulation derived
from the internal carotid arteries (anterior; dark blue) and the vertebrobasilar
arteries (posterior; grey)
Basilar artery
Anterior inferior
cerebellar artery
Vertebral artery
Anterior spinal artery Posterior inferior
cerebellar artery
Posterior circulation
Figure 9.2 The circle of Willis and major cerebral arteries. The hyphenated line
divides the anterior and posterior cerebral circulations.
Lacunar syndrome
A lacunar infarct occurs in the deep penetrating arteries of the
thalamus, corona radiata or internal capsule. Lacunar syndrome
consists of:
• pure motor deficit
• pure sensory deficit
• or both
• it must involve two or more of the face, arm and leg
• no other new neurological symptoms are present
• motor deficit
• sensory deficit
• homonymous hemianopia
• higher cortical dysfunction
Hemispheric dominance
The left hemisphere is dominant and houses language function
in 95% of right-handed people and 70% of left-handed people.
Along with the expected weakness, hemianopia, etc. on the
contralateral side of the body, a stroke in each hemisphere
usually results in quite typical higher cortical dysfunction
(Table 9.3).
Approach
Patients are often dysphasic, disorientated or otherwise unable
to give a reliable history. It is imperative to obtain a collateral
history from family or eye witnesses in order to establish clearly
the timing of onset and any contraindications to thrombolysis.
Telephone family members or witnesses if needed and, if
there is time (e.g. while waiting for a referral to arrive in the
emergency department), contact their relevant healthcare
providers such as GP or other physician to establish premorbid
state, comorbidities or recent interventions. However, do not
delay the rest of the assessment for this.
Sequence
Key information to establish in a stoke history is:
1. the time of onset
• if the patient is unable to clarify, this must be assumed
to be the time last known to be well
• for patients waking up with stroke symptoms this must
be assumed to be when they went to sleep
2. which symptoms are present
• weakness, numbness, speech problems, visual disturbance,
swallowing problems, ataxia, vertigo
3. whether symptoms are improving, worsening or are static
4. risk factors present:
• age
• hypertension
• diabetes
• smoking
• atrial fibrillation
168 Examining the stroke patient
Thrombolysis contraindications
Presentation Onset unclear or more than 3.5 hours ago
Seizure since onset
Invasive/surgical procedure in previous 3 weeks
Cardiopulmonary resuscitation
Pregnancy
Symptoms minor or improving
Significant premorbid dependence.
Bleeding disorder Previous intracranial bleeding
Active bleeding
Active peptic ulcer or gastrointestinal bleeding;
Current anticoagulation use
Cranial disorders Stroke in the preceding 3 months
Head or facial trauma in the preceding 3 months
Structural cerebrovascular disease
Cardiovascular Aortic dissection
Severe hypertension
Diabetic retinopathy
6. medication history:
• full drug history, including recreational drugs
• particularly use of antiplatelet drugs or anticoagulation
• use of insulin or antihyperglycaemic drugs
7. contraindications to thrombolysis (see Table 9.4)
Approach
This is essentially a general neurological examination
aimed at eliciting the major signs required to classify the
syndrome.
170 Examining the stroke patient
Equipment
This requires a tendon hammer, pen torch, hat pin, Neurotip
and tuning fork.
Sequence
To perform a focused stroke examination:
1. assess the Glasgow Coma Scale score
2. orientation: ask the month and the patient’s age
3. commands: ask the patient to open and close their eyes,
then grip and release with their non-paretic hand
4. assess cranial nerves III, IV, VI: note any cranial nerve or gaze palsy
5. assess for visual defects: tested with the hat pin, confrontation
or visual threat as appropriate
• hemianopia
• visual neglect
• visual extinction
6. assess for weakness: face, arms, legs
7. limb ataxia: test finger–nose pointing and heel–shin co-
ordination
8. sensation: test pin-prick sensation or withdrawal to pain
• face
• arms
• legs
• sensory extinction or neglect
• further assess vibration sense when there is clinical
suspicion of a brainstem lesion
9. language: ask the patient to describe what you are wearing,
name items and read a sentence
10. dysarthria: ask the patient to repeat words
11. test the limb and plantar reflexes
Equipment
This requires a stethoscope and an ophthalmoscope.
Sequence
The key body system areas to examine are cardiovascular,
respiratory and gastrointestinal.
Cardiovascular
Assess the following:
• heart rate and rhythm (e.g. atrial fibrillation)
• murmurs (e.g. septic emboli from endocarditis)
• blood pressure (hyper- or hypotension, aortic dissection)
• bruits (poor correlation with carotid artery atheroma)
• fundoscopy (diabetic or hypertensive retinopathy)
• peripheral pulses (vascular disease)
Respiratory
Assess the following:
• respiratory rate (sepsis, pneumonia)
• focal chest signs (aspiration)
Gastrointestinal
Assess the following:
172 Examining the stroke patient
CT
A CT scan should be performed quickly to exclude haemor-
rhage. Note that a CT may be normal early on or in posterior
circulation syndrome infarcts. MRI is far more sensitive and is
indicated if the CT is normal or in posterior circulation syn-
dromes. However, this takes longer than CT and is not usually
available in the acute setting.
An acute ischaemic stroke may appear normal or it may be
evident as:
• sulci effacement: cortical sulci lose definition owing to
subtle oedema
• loss of grey–white differentiation: oedema can cause subtle
loss of distinction between grey and white matter, especially
the lentiform nucleus of the basal ganglia and the cortical
ribbon of the insular cortex
• dense middle cerebral artery (MCA): an occluded MCA can
appear hyperdense on CT, as can an occluded basilar artery
9.7 Thrombolysis
Objective
Alteplase is the treatment of choice for thrombolysis:
• it is licensed for acute ischaemic stroke within 3.5 hours of
onset, although some centres use it beyond this time in a
trial setting
Thrombolysis 173
Approach
The risks and benefits of thrombolysis must be explained to
the patient or next of kin by a physician experienced with its
use. A consultant stroke physician should be consulted prior to
administration.
Equipment
This requires intravenous access and a syringe driver.
Sequence
Alteplase is administered as follows:
1. total dose is 0.9 mg/kg to a maximum of 90 mg
2. initial bolus is 10%
3. remainder infused over 1 hour
4. patient is nursed in a devoted acute stroke unit experienced
in monitoring thrombolysis patients
Examining the 10
coma patient
10.1 Objectives
Key objectives in examining a person in a coma are to assess
the level of consciousness, localise the lesion and detect any
signs of the aetiology. This chapter assumes that the patient
has been resuscitated following standard advanced life support
or advanced trauma life support procedures and is otherwise
stable.
Brainstem lesions
Damage to the brainstem can cause decreased consciousness
along with specific more focal symptoms. The presence of
otherwise normal brainstem function (e.g. reflexes) therefore
points towards a diffuse or cortical cause of decreased
consciousness.
Signs indicating brainstem involvement include the
following.
176 Examining the coma patient
Pupils
Pupil’s can be:
• bilateral pin-point: small, unreactive pupils suggest a
pontine lesion or opiates
• bilateral mid-position: 4–6 mm, unreactive pupils suggest
a midbrain lesion
• bilateral dilated: large, unreactive dilated pupils suggest
anticholinergic poisoning or a preterminal stage of
herniation
Clinical features and pathophysiology 177
Breathing pattern
The patient is likely to be ventilated; nonetheless, the
spontaneous breathing pattern is informative. Ataxic breathing
is a variable amplitude and rate and suggests lower brainstem
dysfunction.
Cortical lesions
Diffuse damage to either or both cerebral hemispheres from
any cause can result in impaired consciousness. The key to
178 Examining the coma patient
Posture
Once admitted to hospital, the comatose patient has meticulous
nursing care directed towards avoiding bedsores. This involves
readjusting posture, so it is often difficult to interpret the
‘natural’ posture of the patient. The following may suggest the
location of the lesion:
• parietal lobe posture: the patient neglects the affected side
and may have their arm or leg in an awkward position
• decorticate posture: in this the patient’s:
– contralateral arm is flexed
– contralateral foot is slightly extended
– eyes are deviated away from the paresis and towards the
hemispheric lesion
• brainstem hemiparetic posture: in this the patient will have:
– Ipsilateral arm and/or leg paresis
– eyes looking towards the lesion and paresis
• decerebrate posture: the patient’s arms and legs are extended
and internally rotated and this indicates a brainstem lesion
Approach
Assuming that the patient has been resuscitated and is stable,
proceed to determine the Glasgow Coma Scale (GCS) score first
to determine how co-operative the patient will be.
Equipment
This requires a stethoscope.
General observations 179
Sequence
Perform a targeted general examination:
1. in an examination situation ask the examiner whether the
patient is otherwise stable and has had their cervical spine
cleared
2. determine their GCS score (Table 10.1)
3. note any intravenous infusions, including sedatives
4. inspect the patient
– skin: cyanosis, pallor, cherry redness, jaundice, petechiae,
uraemic frost
– skull: blood in the ear canal, Battle’s sign, racoon eyes,
cerebrospinal fluid (CSF)
– temperature: pyrexia, hypothermia
– meningism: resistance to passive neck flexion and
extension
Component Score
Eyes open
Spontaneously 4
To verbal stimulation 3
To pain 2
Never 1
Best verbal response
Orientated and converses 5
Disorientated and converses 4
Inappropriate words 3
Incomprehensive sounds 2
No response 1
Best motor response
Obeys commands 6
Localises pain 5
Withdraws to pain 4
Flexes to pain 3
Extends to pain 2
No response 1
Total 15
Approach
Ensure that the C-spine has been cleared of any injury by asking
the examiner or checking X-rays or CT scans.
Eyes and reflexes 181
Equipment
This requires a pen torch, tendon hammer, cotton wool and a
syringe with cold water.
Sequence
To examine the eyes and reflexes of a patient in a coma:
1. note any gaze paresis
2. note any spontaneous eye opening or eye movements
3. open the patient’s eyelids if they are closed and observe
4. ask the patient to look up, down, left, right
5. oculocephalic reflexes: turn the patient’s head to the right,
left, up and down and observe whether their eyes move
6. test the blink reflex
7. note the resting pupil sizes
8. elicit the pupillary reflexes
9. examine tone in the limbs
10. elicit triceps, biceps, knee, ankle and plantar reflexes
11. elicit caloric reflexes if the above fails to demonstrate an
intact brainstem.
Pupils
Pupil signs and their associated lesions are given above in
section 10.3.
Oculovestibular reflexes
These can indicate whether the brainstem is involved or not:
• intact reflex suggests that some basic function of the
brainstem remains
• absent reflexes suggests that the brainstem is involved and
carries a very poor prognosis
The neurological 11
screening
examination
in 4 minutes
11.1 Objectives
There is seldom a good reason not to perform a brief neuro
logical examination on any patient admitted to hospital for
any cause. Even in those without any neurological symptoms
it is important to establish and document baseline gross
neurological function and potentially detect any significant
pathology.
In a busy outpatient setting, many consultant neurologists
only need to perform a very brief screening examination. This
is because they usually already know the diagnosis from the
history (or so they would have you believe!) and are expert at
interpreting any signs that are present.
The following is a simple ordered list of the important
steps to include in such screening examinations. The detailed
techniques are all covered in previous chapters. This may seem
like a lot to do on every patient but, once well rehearsed, such
a screening can be done in 2–3 minutes.
11.2 Sequence
A summary of the sequence of performing a neurological
screening examination is given in Table 11.1.
186 The neurological screening examination in 4 minutes
The neurological 12
examination in
undergraduate
exams
12.1 Objectives
The aim of undergraduate clinical examinations is to ensure
a basic standard of competency and to offer students an
opportunity to demonstrate particular aptitude. Both of these
will only be developed through practice: there is no substitute
for rehearsing the examination routine on real patients. Examin-
ers do not often expect nuanced skill or the ability to discuss
the more subtle points of the neurological examination. Rather,
they want to see students who have a clear grasp of a basic,
but thorough, examination routine.
For those students with a keen interest in neurology or
a wish to excel in the clinic examination, the key is to be
sufficiently practised in the routines described here to be
able to carry them out correctly and quickly in order to spend
more time on questions with the examiners. Spending time
attempting to elicit fine points of the examination is less
impressive than finishing quickly, having a sensible summary
and differential, and then being able to discuss investigations
and management.
So the key to basic competency is practice, and the key to
standing out is even more practice! In the immediate run-up to
examinations it is often helpful to pair up and examine a fellow
student repeatedly until the routine is slick, fast and second
nature. Of course, without seeing real patients beforehand,
any real signs found in the actual examination will prove more
difficult to interpret.
188 The neurological examination in undergraduate exams
Neuroanatomy
Haines DE. Neuroanatomy: An Atlas of Structures, Sections and Systems. Philadelphia:
Lippincott Williams & Wilkins, 2003.
Hirsch M, Kramer T. Neuroanatomy: 3-D Stereoscopic Atlas of the Human Brain. Berlin:
Springer, 1999.
Basic neuroscience
Cooper JR, Bloom FE, Roth RH. The Biochemical Basis of Neuropharmacology, 8th edn.
New York: Oxford University Press, 2003.
Kandel E, Schwartz, JH, Jessell TM. Principles of Neural Science, 4th edn. New York:
McGraw-Hill, 2000.
Shephard GM. The Synaptic Organization of the Brain, 5th edn. New York: Oxford
University Press, 2004.
Psychiatry
Burton, N. Psychiatry, 2nd edn. Oxford: Wiley-Blackwell, 2010.
Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading
the cognitive state of patients for the clinician. J Psychiatr Res 1975;12:189–98.
Mind–brain philosophy
Eccles JC, Popper K. The Self and Its Brain. Abingdon, UK: Routledge, 2003.
Index
Note: Page numbers in bold or italic refer to tables or figures respectively.
Frontalis muscle, 65 H
Frontal–temporal dementia, 141 Haemorrhagic stroke, 164, 169
Frontotemporal dementia, 147 Hallpike’s manoeuvre, 69
Fundi, in CN II assessment, 58 Hallucis longus flex, 108
Fundoscopy, 52, 55 Handedness, 186
ophthalmoscope adjustment, 55 Head and neck, 27
CN I (olfactory nerve), 27
G CN II (optic nerve), 28, 38–42
Gag reflex test, for mouth, 72 CN III, IV and V (eye muscle nerve), 29,
Gait, 186 31, 44–5
abnormal posture and movements, CN IX (glossopharyngeal nerve), 34–6,
18–22 47–8
assessment, 22–5, 27 CN V (trigeminal nerve), 31, 46
asymmetrical gait, 16–17 CN VII (facial nerve), 31, 34
basal ganglia/extrapyramidal system, CN VIII (vestibulocochlear nerve), 34,
10–11, 12 47
broad-based symmetrical gait, 15–16 CN X (vagus nerve), 36, 47–8
in CN VIII assessment, 75 CN XI (accessory nerve), 36, 48
cerebellum, 11 CN XII (hypoglossal nerve), 36, 48–9
functional gait, 17 ears, CN VIII, 67–70
general inspection, 12–16, 27 eyes, CN II and III, 52–8
narrow-based symmetrical gait, 16 eyes, CN III, IV and VI, 59–62
pyramidal system, 10 face, CN V and VII, 62–7
sensory input, 9–10 mouth, CN IX, X, XII, 71–3
Gastrocnemius, plantarflexes, 108 neck, CN XI, 73–5
Gaze paresis, 181 nose, CN I, 50–1
Generalised wasting papillary reflexes, 36–8
in head and neck, diagnosis, 50 pupil, 42–3
Glasgow Coma Scale (GCS) score Head drop, 50, 73
in coma patient, 178, 179 Head rotated, 50
in stroke assessment, 170 Head tilted, 50
Glaucoma, 58 Head turning test, in CN VIII assessment,
Global encephalopathies, 140 69–70
Glossopharyngeal nerve (IX), 34–6 Headaches, 3, 132, 133
lower cranial nerves, mouth, 30 haemorrhagic stroke, 169
Glossopharyngeal neuralgia history of, 188
peripheral, 73 Heart rate variability
Glove and stocking, in paraesthesia, 87 as ANS abnormality, 155–6
Gluteal nerve, 105, 106 Heel–shin, co-ordination, 119
peripheral nerve, of lower limb, 106 Hemiballismus, 11
Gluteus maximus (GluMax), 106 Hemiplegia
Gluteus medius (GluMe), power, 106 in head and neck, diagnosis, 50
Gluteus minimis (GluMi), power, 106 in gait assessment, 16, 23
Guillain–Barré syndrome, 5, 39, 49, 73, Hemi-sensory distribution, in
158, 188 paraesthesia, 87
198 Index