JINKINS • • (Editors) EMERGENCY NEURORADIOLOGY ii edizione With 294 Figures in 793 Parts and 10 Tables EDITORS Tommaso Scarabino Department of Neuroradiology, Scientific Institute “Casa Sollievo della Sofferenza”, San Giovanni Rotondo (FG), ITALY Department of Radiology, ASL BA/1, Hospital of Andria (BA), ITALY Ugo Salvolini Neuroradiology and Department of Radiology, University of Ancona, ITALY J. Randy Jinkins Department of Radiology, Downstate Medical Center, State University of New York, Brooklyn, NY, USA This edition of Emergency Neuroradiology by Scarabino – Salvolini – Jinkins is published by arrangement with Casa Editrice Idelson-Gnocchi srl, Naples, Italy ISBN-10 3-540-29626-3 Springer Berlin Heidelberg New York ISBN-13 978-3-540-29626-3 Springer Berlin Heidelberg New York Library of Congress Control Number: 2005934099 This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilm or in any other way, and storage in data banks. Duplication of this publication or parts thereof is permitted only under the provisions of the German Copyright Law of September 9, 1965, in its current version, and permission for use must always be obtained from Springer-Verlag.
Violations are liable for prosecution under the German Copyright Law. Springer is a part of Springer Science+Business Media http://www.com © Springer Berlin Heidelberg 2006 Printed in Germany The use of general descriptive names, registered names, trademarks, etc. in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. Product liability: The publishers cannot guarantee the accuracy of any information about the application of operative techniques and medications contained in this book.
In every individual case the user must check such information by consulting the relevant literature. Ute Heilmann Desk Editor: Meike Stoeck Production Editor: Joachim W. Schmidt Cover Design: eStudio Calamar, Spain Typesetting: FotoSatz Pfeifer GmbH, 82166 Gräfelfing, Germany Printed on acid-free paper – 24/3151 – 5 4 3 2 1 0 CONTRIBUTORS R. Zarrelli FOREWORD Encouraged by the success of the Italian editions, the Authors have decided to publish an English version taking into account the latest technical and methodological advances and the consequent new acquisitions in clinical practice.
The contribution of Professor R. Jinkins has been essential to carry out both these tasks. The resulting work is an up-to-date technical tool that preserves its original aim of contributing to the training of those radiologists who work in emergency departments. We hope that this revised and extended English version will have the same success as the previ- ous Italian editions, thereby confirming the validity of our initiative.
The work of all the friends and colleagues who have contributed to the making of this book is gratefully acknowledged. Tommaso Scarabino Ugo Salvolini CONTENTS I.1 Clinical and diagnostic summary Neuroradiological protocol .2 CT in ischaemia Introduction. 7 Particular forms of infarction .3 CT in intraparenchymal haemorrhage Introduction. 27 The role of CT.
34 Particular forms of IPH .4 CT use in subarachnoid haemorrhage Introduction. 58 Postsurgical follow-up .5 MRI in ischaemia Introduction. 64 Possible uses of clinical MR in the diagnosis of emergency ischaemia after the hyperacute phase .6 Functional MRI in ischaemia Introduction .7 MRI in haemorrhage Introduction .9 MR angiography Introduction. 102 MR angiography of the supraaortic vessels .10 Conventional angiography Introduction .1 Clinical and diagnostic summary Neuroradiological protocols .2 CT in head injuries Introduction .3 MRI in head injuries Introduction .4 CT in facial trauma Introduction.
179 CONTENTS XI Techniques .1 Pathophysiology and imaging Introduction. 195 The pathophysiology of intracranial hypertension. 201 ICH related to abnormal CSF physiology. 203 ICH related to vascular causes.
210 Aetiological causes of intracranial hypertension .2 Neoplastic craniocerebral emergencies Introduction. 213 Imaging examination technique. 214 Posttherapeutic neoplastic emergencies .3 Angiography in brain tumours Introduction. 233 Other cerebral neoplasms .1 Toxic encephalopathy Introduction.
246 Ethylene-glycol intoxication. 246 Intoxication from narcotic inhalation. 246 Intoxication from medicines. 247 Carbon monoxide (CO) intoxication .2 The neuroradiological approach to patients in coma Introduction.
253 Modes of intracranial analysis. 258 Acute primary focal cerebral lesions. 259 Widespread insult/brain swelling .3 Nuclear medicine in neurological emergencies Introduction. 265 XII CONTENTS Measuring CBF.
266 Clinical usage of HM-PAO SPECT .4 Diagnosing brain death Introduction .5 Postsurgical craniospinal emergencies Introduction .1 Clinical and diagnostic summary Neuroradiological protocols .2 CT in spinal trauma emergencies Introduction .3 MRI in emergency spinal trauma cases Introduction .4 Emergency imaging of the spine in the non-trauma patient Introduction. NEUROPAEDIATRIC EMERGENCIES Introduction .1 CLINICAL AND DIAGNOSTIC SUMMARY T. Maggialetti Stroke, a clinical diagnosis of acute, sudden- porally worsening clinical condition during the onset neurological deficit, is one of the main first 24 to 48 hours following acute onset asso- causes of death and permanent disability in the ciated with persistent functional deficit; com- industrialized world. Pathologically the process plete ictus is a clinically stable condition, with may be an ischaemic or a haemorrhagic event, the deficit being present from the outset, or both.
About 85% of cerebrovascular acci- though some improvement may be observed in dents result from ischaemia, predominantly the long term. secondary to carotid thromboembolism. The stroke patient may clinically present with typical symptoms of focal neurological NEURORADIOLOGICAL PROTOCOL deficit, a combination of deficit with coma, a meningeal irritation syndrome in the form of The role of the neuroradiologist in stroke headache, vomiting and neck stiffness, or less cases is to provide the clinician with the maxi- frequently with the gradual appearance of an mum morphological and functional informa- extrapyramidal or pseudo-bulbar syndrome of- tion concerning the condition of the cerebral ten associated with progressive mental deterio- parenchyma as is possible, as well as the condi- ration. tion of the intra- and extracranial brachio- The clinical picture in stroke patients can be cephalic blood vessels.
One should particularly classified according to how long the neurologi- assess whether or not there is a direct causal re- cal deficit lasts, or alternatively whether or not lationship between the craniocervical vascular the deficit is permanent. Four different such pattern and the stroke, whether the lesion is is- clinical categories can be distinguished. The chaemic or haemorrhagic, if there are signs of transient ischaemic attack (TIA) is represented other vasculopathic changes, and if the aetio- by a sudden, focal non-convulsive onset of a logic factors responsible for the stroke are in- neurological deficit that usually subsides in a tra- or extracranial. few minutes and always resolves within 24 The recent development of specific fibri- hours; the reversible ischaemic neurological nolytic treatments that can potentially reverse deficit (RIND) lasts at most for a period of 48 ischaemic injury in the early stages has changed hours followed by a return to complete nor- the role of imaging in this area (5).
It is no mality within 3 weeks; progressive ictus is a tem- longer sufficient to simply distinguish is- 4 I. CEREBROVASCULAR EMERGENCIES chaemic alteration from primary haemorrhage. mediately after the bleeding episode due to its It is now necessary to identify cerebral is- high density relative to brain tissue. However, chaemia within the first few hours when treat- haemorrhage has a more complex appearance ment can be most effective.
It is also important and explanation on MRI. An acute cerebral to quickly distinguish normal cerebral tissue haemorrhage is primarily oxyhaemoglobin, a from that which is “at risk”, and that parenchy- substance with no paramagnetic properties that ma which is irreversibly damaged. Thus, the behaves much like an aqueous solution, almost medical imaging investigation is now a funda- indistinguishable from an area of parenchymal mental part of planning effective emergency ischaemia. In subacute haemorrhage, the treatment potentially capable of preventing ir- parenchymal blood that was originally oxy- reversible cerebral damage and long-term pa- haemoglobin first turns into deoxyhaemoglo- tient disability.
The neuroradiologist must bin, and then into intracellular and next into therefore find the optimal means of supplying extracellular metahaemoglobin. These sub- the required information through both invasive stances are paramagnetic and/or magnetically and non-invasive investigative methods. susceptible and therefore are able to influence Angiography has to date been the most com- relaxation times and change the MR signal in a monly used of the available tools to analyse the somewhat predictable manner. brachiocephalic vascular system directly.
Less Recently released high field strength, high invasive methods include computed tomogra- speed MR equipment and imaging sequences phy (CT), ultrasound and magnetic resonance are particularly sensitive to magnetic suscepti- imaging (MRI), both conventional (basic mor- bility differences (e., echo planar imaging: phological imaging and angiography) and func- EPI) has demonstrated that it is possible to tional (spectroscopy, diffusion and perfusion). clearly reveal even small areas of cerebral haem- Single photon emission computed tomography orrhage on MRI (15). Because of this ability of (SPECT) and positron emission tomography MRI to distinguish between non-haemorrhagic (PET) are able to show local changes in blood ischaemia and haematoma, MRI may replace flow and metabolism, respectively, both mark- CT at some time in the future where this is prac- ers for cerebral damage. However, these latter ticable.
However, the fact that high field methods are not commonly available, and re- strength, high speed gradient performance MRI quire the injection of radioactive tracers. is presently less widely available and more cost- In emergency situations, the cerebral investi- ly than CT determines that CT will still be the gation of choice is CT due to its non-invasive- first diagnostic imaging examination carried out ness, the fact that it is widely available, its ease in such situations for the foreseeable future. On and speed of use and its relatively low cost (7). the other hand, emergency angiography should CT distinguishes between haemorrhagic and is- be reserved for cases of subarachnoid haemor- chaemic stroke at an early stage, a factor that rhage in order to search for causative pathology may be of vital importance in prognosis and of stroke (i., haemorrhage) such as aneurysms treatment.
If the CT is negative or incongruous or vascular malformations (3). in some way with the clinical picture, MRI makes possible a more detailed brain investiga- tion to be carried out non-invasively. ISCHAEMIC STROKE CT has been shown to be unable to document HAEMORRHAGIC STROKE the presence of non-haemorrhagic ischaemic al- teration in the first few hours following the clini- CT has always been considered useful in cal onset of stroke. Over a period of hours and analysing cerebral haemorrhage, whether sub- with proper experience, it is in practice possible arachnoid or intraparenchymal in location.
In- to identify the subtle initial signs of ischaemic tis- tracranial haemorrhage is apparent on CT im- sue damage as relatively lower attenuation brain 1.1 CLINICAL AND DIAGNOSTIC SUMMARY 5 tissue resulting from cytotoxic oedema, and ma- acute clinical stage is imperative (1). With MR jor cerebral arterial hyperdensity (e., middle angiography it is possible to evaluate the arteri- cerebral artery stem, basilar artery) due to vascu- al anatomy of the major vessels at the base of lar embolus/thrombosis (12, 14, 16). Good anatomical imaging shows ei- Although conventional T2-weighted MRI ther the normal vessels composing the circle of (e., spin echo, fast spin echo) is particularly Willis, or their absence in the ischaemic cere- sensitive to changes in the water content of tis- bral area. This may at times be the key to the di- sue and therefore to oedema, it is still frequent- agnosis of major vascular occlusion, in which ly negative in cases of hyperacute stroke (i., case it is useful to extend the MR angiographic first 1-6 hours).