Neurological Skills. A Guide to Examination and Management in Neurology PDF
Preview Neurological Skills. A Guide to Examination and Management in Neurology
To Heather, John and Iain Neurological Skills A Guide to Examination and Management in Neurology Michael J.G. Harrison, DM, FRCP Professor in Clinical Neurology and Francis and Renee Hock Director of Research, Reta Lila Weston Institute of Neurological Studies, University College and Middlesex School of Medicine Butterworths London Boston Singapore Sydney Toronto Wellington ^ PART OF REED INTERNATIONAL RL.C. All rights reserved. No part of this publication may be reproduced in any material form (including photocopying or storing it in any medium by electronic means and whether or not transiently or incidentally to some other use of this publication) without the written permission of the copyright owner except in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of a licence issued by the Copyright Licensing Agency Ltd, 33-34 Alfred Place, London, England WC1E 7DP. Applications for the copyright owner's written permission to reproduce any part of this publication should be addressed to the Publishers. Warning: The doing of an unauthorised act in relation to a copyright work may result in both a civil claim for damages and criminal prosecution. This book is sold subject to the Standard Conditions of Sale of Net Books and may not be re-sold in the UK below the net price given by the Publishers in their current price list. First published 1987 Reprinted 1990 © Butterworth & Co. (Publishers) Ltd, 1987 British Library Cataloguing in Publication Data Harrison, Michael, 1936- Neurological skills : a guide to examination and management in neurology. 1. Neurology I. Title 616.8 RC346 ISBN 0-407-01360-1 Library of Congress Cataloging in Publication Data Harrison, M. J. G. (Michael J. G.) Neurological skills. Includes bibliographies and index. 1. Nervous system—Diseases—Diagnosis. 2.Nervous system—Diseases. I. Title. [DNLM: 1. Nervous System Diseases—diagnosis. 2. Nervous System Diseases—therapy. 3. Neurologic Examination. WL 141 H321n] RC348.H316 1986 616.8Ό475 86-20720 ISBN 0-407-01360-1 Typeset by Scribe Design, Gillingham, Kent Printed and bound by Butler and Tanner Ltd, Frome and London Preface The ability to make a neurological diagnosis Hopefully, the illustrations and text that depends above all on the capacity to under- follow will help the student, at whatever stand the patient's history, to carry out a stage, to gain confidence in his or her ability reliable examination and to interpret neurolo- to cope with neurological problems; to lessen gical symptoms and signs. This book the mystery of neurology without losing any attempts to describe the neurological ex- of its fascination. amination and its pitfalls and discusses how To simplify the text, the patient has been physical signs or lack of them can be used to referred to as 'he' throughout, although cases substantiate or refute the hypothesis gener- occur in both sexes. So that subsections can ated whilst listening to the patient's own be consulted in isolation, there is some account of affairs. First steps in the manage- repetition of key points. ment of neurological conditions are also described. Acknowledgements It is a pleasure to record my gratitude to retinal photographs. Permission to reproduce Charles Fry and Sue Deeley of Butterworths figures was kindly granted by the Oxford and to Marie-Louise Autin and Beryl Laatz University Press, the editors of the Oxford who patiently oversaw the gestation of the Textbook of Medicine and the publishers and manuscript. I must also express my thanks to editor of the British Journal of Hospital Medi- the authors of many fine monographs, to all cine, the Physician, and the British Medical my teachers, and students, and to my patients Bulletin. I am grateful to Dr Ben Aspey and to who all provided moments of insight. Their the staff of the Department of Medical sagacity accounts for many useful tips, the Illustration of the University College and errors are mine. Dr Michael Johnson read the Middlesex School of Medicine for their skilled text and made many useful suggestions. Mr assistance with the figures and tables. Peter Hamilton kindly provided some of the 1 History and examination The history example, if it sounds as though the patient may have spinal cord disease, one would go on to ask about back pain and sphincter Taking a revealing history is a highly skilled disturbance if these had not yet been men- exercise. Although it is learnt largely by tioned. By showing interest and sympathy at apprenticeship, some advice can be prof- this stage one is also building a rapport that fered. will be vital to the patient's compliance with It is important to secure the patient's trust advice or medication, and trust in the and allay his nervousness by a friendly diagnosis. approach and due privacy. A history taken in As well as giving clues about the function the open ward is unlikely to be given in a or part of the neuraxis at fault, the history relaxed way, and so may be unreliable. The also reveals most of the information needed examiner must hide his irritation at vague- to diagnose the nature of the pathological ness and his hurry. The patient must feel that process responsible for the symptoms. Thus this doctor will listen, and has time to hear the nature of the onset and the time course of him out. This means that a mental note must evolution of symptoms reveal whether the be made of matters that will need clarification patient has a vascular or mechanical lesion by gentle probing, and the patient initially (sudden onset), an inflammatory disease allowed to get off his chest those things he (usually subacute onset over days) or a most wants the doctor to hear. Later it is neoplastic or degenerative disorder (insi- appropriate to discourage a catalogue of dious onset with progresive deterioration). second-hand medical opinions from previous Intermittent processes like those in multiple consultations, and to analyse what the sclerosis, epilepsy and migraine produce a patient has meant by words like numb, or diagnostically episodic history. dizzy. However, care must be taken not to The history also directs the subsequent 'lead the witness' by suggesting answers to examination. At the end of the history it important questions. should be clear which parts of the neurologic- As one listens it is important to start al examination are going to be crucial. The hypothesizing about the meaning of the examination 'digs' where the history has history taken. What is the anatomical im- marked an 'Χ', or rather a '?'. In addition the plication of the presenting symptom or group examiner will be intent on ruling out other of symptoms; does it sound like a disorder of possibilities, as well as confirming the first consciousness, of the vestibular or visual hypothesis. Alternative diagnoses that re- system, of motor or sensory function, etc.? quire very different management or treat- The hypothesis should only be vague but it ment must always be considered, if only to be will be important in directing the later refuted. questions aimed at clarification and at con- It should be clear that history taking is an firming or refuting the initial localization. For active process, the examiner processing the 1 2 History and examination information, formulating a hypothesis or gives the history without moving his mouth several hypotheses, rejecting some as further more than a fraction, and who points to the data appear and planning the examination. site of the pain without daring to touch the Research has shown that the experienced pointing finger on the face, has trigeminal clinician makes his first hypothesis, albeit a neuralgia. Such a spot diagnosis is not often fairly vague one, within seconds of meeting possible, however, and routine questions are the patient. needed both of nervous system function, and The clues are not only those of the stated of the health of other systems (Table 1.1). history. While the patient is being greeted, Table 1.1 Routine neurological enquiry seated, and invited to explain his problem, Have you noticed any change in your mood, the clinician has an opportunity to start the memory or concentration? examination. The patient reveals much of his Is your sleep disturbed? personality, mood, intelligence, memory, Have you had any black-outs or been dizzy? language, and voice as he tells his story. Have there been any problems with vision, Body language is also revealing. The patient's hearing or balance? agitated or depressed mood affects his Have you had difficulty with talking, chewing or movements. Some neurological conditions swallowing? may be suspected on first meeting the Have you noticed any numbness or pins and patient. The walk as the new patient needles in your face, body, arms or legs? approaches the desk may reveal parkinson- Have you had weakness, heaviness or clumsiness ism, hemiplegia, ataxia or foot drop. The of your limbs? Is your walking affected? difficulty getting out of the chair at the end of Have you normal control over your bowels and the interview may alert one to the possibility waterworks and is sexual function normal? of proximal muscle weakness. The general appearance of the face may suggest an Problems may arise because the patient is endocrine abnormality (hypopituitarism, unintelligent, dementing, deaf, depressed or acromegaly, hypothyroidism, exophthalmic frightened, or has a language disorder (dys- goitre) or reveal a rash (adenoma sebaceum, phasia). The doctor may be tired, have a lupus pernio, disseminated lupus erythema- headache, or be inattentive or interrupt too tosis, dermatomyositis)—all clues to the often. If not careful he may put words into neurological condition. A parkinsonian im- his patient's mouth in an attempt to save time mobility or a weak face may be obvious and and cut corners. The solution may be to start disorders of the eyelids or eyes can be again on another occasion. All junior doctors noticeable as the patient is questioned. A tilt know the irritation of hearing a patient of the head may suggest cervical disc disease, produce a new gem of information when a posterior fossa tumour, or diplopia due to telling his story to the consultant, which he weakness of one of the oblique muscles. forgot or was insufficiently encouraged to Parkinsonian tremor may become obvious in reveal when first encountered. The other aid the hand resting on the lap. to overcoming these difficulties is to inter- For all these reasons, and to increase view a relative as well. Besides confirming rapport, as well as to be polite, the clinician the accuracy of the patient's own story, such should look at the patient's face while additional history may also reveal the pa- listening. Note taking should be limited and tient's lack of memory or a change of saved until later. The patient who is talking personality. Eyewitness accounts of attacks to a doctor who has his head in the notes of loss of consciousness, for example, are scribbling furiously is unlikely to relax and worth miles of EEG recording, so patients fully co-operate, and the doctor will be with black-outs must be asked to bring an missing some valuable physical signs. eyewitness to the consultation if at all The act of making a diagnosis is frequently possible. A phone call to a relative, work- one of pattern recognition. The patient who mate, or doctor may not be a glamorous way describes sharp stabs of pain in one side of of making a diagnosis but can be very 'cost the face provoked by eating and talking, who effective'. The general examination 3 Some features of the history suggest that suggests open sutures, for example in an the patient will be unlikely to have any infant with hydrocephalus, and unilateral evidence of organic disease. The patient may dullness may indicate a subdural collection. show either exaggerated distress, or demons- The spine too is percussed for focal tender- trate 'la belle indifférence''. A shopping list of ness suggesting local pathology such as an medical consultations or symptoms, or a epidural abscess, or vertebral metastasis, and bizarre symptom, may arouse suspicions in observed and palpated for any hint of the clinician's mind. Discrepancies may also scoliotic curvature. Such a curve may be be obvious in the patient's appearance. A congenital or part of a hereditary condition woman with difficulty in using her hands is such as Friedreich's ataxia, but may also be unlikely to be accurately made up. Well- acquired from muscle paralysis as in brushed hair may conflict with a complaint poliomyelitis or with skeletal disease. A tuft that the arms cannot be lifted above shoulder of hair or dimple in the lumbar region may be level. a clue to a congenital spinal abnormality such Finally one should recall probabilities. as spina bifida. Most headaches will be due to migraine or The size of the two hands and feet should tension, for example. This does not mean be compared by placing them side by side. A that other important causes must not be hemiparesis in infancy may be reflected in considered and excluded but it does mean retarded growth on one side. The length and that the clinician's 'bias' should be towards girth of thumbs or fingers or the length and the likely, not the unlikely. width of the foot may reveal a difference. The patient may know that they need a half size smaller shoe on one side. A high arched foot Further reading under which a light can be seen from the side even when a flat board is pressed up onto the heel and sole can be a sign of other congenital BALLA, j.i. (1980) Pathways in Neurological Diagnosis. Edward Arnold, London. anomalies or hereditary conditions. Such a pes cavus is found, for example, in some hereditary neuropathies. The toes tend to be bunched up. Examination of the skin may yield useful The general clues. Many café-au-lait patches are indica- tive of neurofibromatosis even when there examination are no obvious fibromas or neuromas. Rashes about the face may indicate tuberose scler- osis, or dermatomyositis and the fine pale texture of the skin of a patient with pituitary The routine physical examination including failure may prompt a survey of body hair and obligatory measurement of the blood press- testicular size. ure may of course reveal the cause of Neck stiffness is sought by passive flexion neurological problems but will not be consi- of the neck by the examiner's hands under dered in detail. Clearly a hard prostrate, a the occiput. This is best done from directly in breast lump, lymphadenopathy, a cardiac front with the elbows flexed. Limitation source of embolism, or signs of organ failure suggests meningitis or subarachnoid bleed- may all be crucial. Some aspects of the ing. If lateral flexion of the neck is restricted, examination are more directly relevant to the cervical spondylosis is the likely cause. A making of a neurological diagnosis, however, general rigidity is felt in some parkinsonian and will be discussed. syndromes. Limitation of elevation of the The skull should be palpated for lumps or extended leg with the examiner's hand under bulges (over a meningioma), its circumfer- the heel implies root irritation, for example ence measured if hydrocephalus is sus- by a prolapsed disc, or meningeal irritation. If pected, and percussed. A cracked-pot note the flexed knee is brought up to the abdomen 4 History and examination and then the knee is extended, resistance is depressed, thought disordered, confused, felt again with meningism or root entrapment amnesic or overtly demented. More formal (Kernig's sign). assessment may need the skills of a clinical A bruit may be heard over cranial arter- psychologist, but an intermediate level of iovenous malformations or fistulae; it is best testing at the bedside by the clinician is an sought by placing the bell of an Old- important part of the neurological fashioned' stethoscope over the closed eye. examination. The patient should be asked to open the other eye and fix his gaze so that movement Dysphasia of the eyeball under the stethoscope does not cause uninvited extraneous noises. Bruits over the neck commonly arise from the heart. Listening to the patient's speech and observ- If this is the case they will be recognized over ing his comprehension of what he hears will the precordium and heard in the sternal give an impression of language capability. notch and will peter out somewhat as they This is preferable to trying to take a short cut are conducted up the major vessels. A bruit and testing naming ability, which can be restricted to the angle of the jaw is likely to be mildly defective in confused patients when it a marker of atheromatous stenotic disease of does not prove that the dominant hemis- the carotid artery. Venous hums have a lower phere is damaged. The ability to read, write frequency, vary with head position and and repeat words and phrases should be posture, and may be stopped by gentle tested. Lesions in the frontal lobe produce a pressure on the neck or by a Valsalva non-fluent disturbance of speech. The patient manoeuvre. A thyrotoxic goitre may also be comprehends normally but produces few the source of a continuous murmur. Au- words or telegrammatic short sentences. The scultation over the spine may extremely speech lacks melody and rhythm. Proposi- rarely reveal the bruit of a spinal angioma, tional speech is lost before expletives. Be- and is worth carrying out in patients with a cause Broca's area for speech is close to the spinal lesion. face and mouth area of the motor strip, there Joint disease may impair movement and may be some difficulty pronouncing some complicate testing of muscle power so the full syllables due to a 'high level' disturbance of range of passive movement at joints like the complex muscle activity needed for articula- shoulder and knee may have to be checked. tion. When there is a temporal lobe lesion causing dysphasia the speech is fluent Swelling and abnormal mobility may be though full of errors (Wernicke's aphasia). found in a Charcot joint, disorganized by loss Many words are incorrect (paralogisms) and of pain sensibility as in syringomyelia, tabes some are apparently newly invented ones dorsalis or diabetes mellitus. (neologisms). The normal cadence of speech is preserved (prosody) and the patient sounds as though he is talking in an unfamiliar language. To add to this impress- The neurological ion he fails to understand the spoken word. Extensive lesions of the dominant hemis- examination phere may affect both the temporal and frontal areas involved in language function. The resultant global dysphasia is non-fluent Mental state and language and the patient is also unable to understand. Rare disconnections of these two speech areas, for example by lesions in the parietal The patient's appearance, demeanour and lobe, produce a fluent dysphasia with re- performance during history taking are them- latively preserved comprehension but a great selves good tests of intelligence, memory and difficulty in repeating phrases (conduction behaviour. Whilst the history is given it may aphasia) (Table 1.2). become clear that the patient is anxious, The neurological examination 5 Table 1.2 Types of dysphasia Type Site of Features lesion Output Comprehension Other 1. Broca Frontal Non-fluent Good Hemiplegia 2. Wernicke Temporal Fluent Bad Field defect 3. Conduction Parietal Fluent Good Cannot repeat 4. Global Combined Non-fluent Bad Hemiplegia Hemisensory loss Field defect Other faculties dominant side a special difficulty with dres- sing may occur and denial and neglect of the The detection of dysphasia of whatever type opposite limbs are likely. On the dominant defines a lesion in the dominant hemisphere side difficulty with calculations, right-left which is on the left in some 95 per cent of the orientation and writing are seen (Ger- population. Other neuropsychological de- stmann's syndrome). A lesion of the left ficits that implicate the left hemisphere angular gyrus causes striking difficulty with include difficulties with calculation and ver- reading. Contralateral sensory disturbance is bal memory. Right-sided lesions should be usually detectable. suspected if the patient has lost visual Occipital lobe lesions, as well as causing memory, has difficulty with visuospatial field defects, impair colour recognition and tasks such as dressing and finding his way, the identification of objects from their visual or shows striking neglect or denial of the left image. Bilateral damage to the visual cortex side (anosognosia). causes blindness with loss of optokinetic Frontal lobe lesions cause personality nystagmus. The patient may deny blindness change with apathy or disinhibited silliness. (Anton's syndrome). The patient may be incontinent and may Table 1.3 sets out the neuropsychological have a grasp reflex—when the examiner 'scan' which provides localizing evidence. draws his fingertips down the palm and on to Global impairment of such functions, espe- the palmar aspect of the patient's fingers they cially of learning and memory, imply demen- curl to grip his hand against an adducted tia. Simple tests of general knowledge, the straight thumb. A subfrontal tumour such as ability to calculate, learn a name and address a meningioma may cause tell-tale anosmia, or and recall it at 3 minutes, and learn and optic atrophy on one side (the side of the reproduce an abstract Binet figure will reveal mass) and papilloedema on the other—the modest impairment. Severe degrees of de- Foster-Kennedy syndrome. Seizures are mentia are obvious when the patient cannot common and often versive in type with head name the day and date, identify where they and eyes turning away from the side of the are, or give an account of themselves. Formal irritative lesion. Status epilepticus in a patient psychometry is necessary when there is any who has never had a fit before is often due to uncertainty, especially when there is a a frontal lobe lesion. problem in distinguishing depression from Temporal lobe lesions are characterized by dementia. A mini-mental state examination memory problems, Wernicke's aphasia, visual can be used to quantitate moderate dementia field defects and seizures affecting smell, at the bedside (Table 1.4). taste, visual, auditory or bodily sensations. Confusion superficially resembles demen- Parietal lobe lesions cause difficulties with tia but the history is short and the patient is performance of complex acts (praxis) such as agitated and hallucinated. His attention span striking a match despite adequate muscular is short, and consciousness level mildly power and co-ordination. On the non- impaired. There is rich detail in confused
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