Clinical Methods In Pain Medicine 2nd Edition 2018

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Clinical Methods in

Pain Medicine

~

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-

~

~ CBS

CBS Publishers & Distributors Pvt Ltd

G·alwifam Das

Clinical Methods in

Pain Medicine Second Edition

Editorial Board

Co-Editors

Tinni T. Maskoen Indonesia ([email protected]. id)

Chinmoy Roy

Kawsar Sardar Bangladesh ([email protected]) Eltayeb Abdulrahman Abdul Gadir Sudan ([email protected]) Awisul lslah Ghazali Malaysia (ghazali_ [email protected]) Chen Chee Kean Malaysia ([email protected]) Chilafat Dalimuthe Indonesia ([email protected]) Ngurah Ketut Indonesia ([email protected]) Debjyoti Dutta MD, FIPP Director, Samabyathi Pain Clinic, Kolkata Kanchan Sharma MD, FIPM Diector, Aaadhya Pain Management Center, Jaipur

MD FIPP

Consultant Pain Physician Institute of Neurosciences Kolkata, India R Gurumoorthi MD Director, Dr Guru's Pain Clinic Trichy, Visiting consultant, Daradia-The Pain Clinic, Kolkata, India Samarjit Dey MD Department of Anesthesiology JIPMER, Puducherry India Polak Mehta MD, FIPP Director Pain Care Clinic Ahmedabad

Clinical Methods in

Pain Medicine Second Edition

Editor

Gautam Das Mo FIPP Chief Executive Editor Indian Journal of Pain Director Daradia-The Pain Clinic Course Director Daradia Pain Management Courses Kolkata

IJ CBS

CBS Publishers & Distributors

Pvt Ltd

New Delhi • Bengaluru • Chennai • Kochi • Kolkata • Mumbai Hyderabad • Nagpur • Patna • Pune • Vijayawada

Disclaimer cience and technology are constantly changing fields. New research and experience broaden U1e scope of information and knowledge. The authors have tried their best in giving information available to them while preparing the material for U1i book. Although, all efforts have been made to ensure optimum accuracy of the material, yet it is quite possible some errors might have been left uncorrected. The publisher, the printer and the authors will not be held responsible for any inadvertent en-ors, ormsstons or inaccuracies. eISBN: 978-81-239-xxxx-x Copyright© Authors and Publisher First eBook Edition: 2017 All rights reserved. No part of this eBook may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system without permission, in writing, from the authors and the publisher. Published by Satish Kumar Jain and produced by Varon Jain for CBS Publishers & Distributors Pvt. Ltd. Corporate Office: 204 FIE, Industrial Arca, Patparganj, New Delhi-I l 0092 Ph: +91-11-49344934; Fax: +91-11-49344935; Website: www.cbspd.com; www.eduport-global.com; E-mail: eresources(a)cbspd.com; [email protected] Head Office: CBS PLAZA, 4819/XI Prahlad Street, 24 Ansari Road, Daryaganj, New Delhi- I I 0002, India. Ph: +91-l l-23289259, 23266861, 23266867; Fax: 0l 1-23243014; Website: www.cbspd.com; E-mail: [email protected]; [email protected].

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Representatives Hyderabad Pune Nagpur Manipal Vijayawada Patna

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Contributors Chapter

Gautam Das

1, 2

gdas23 I [email protected]

Kanchan Sharma

l , 11 2, 10 2 3, 7, 12 3,6,9, 15 4,5 5

[email protected]

12

Sourav lswarari

13, 14

Aniketa Banerjee

13

Saikat Majumdar

13

Dibyendu Das

14

[email protected]

6,9, 15

[email protected]

Samarjit Dey

Mirghani Ali

[email protected]

[email protected]

Tarun Kumar Reddy

11

aniketa. banerjee. ko/[email protected]

drbhavnaboro/[email protected]

Mamta Mishra

Karthic Babu N

[email protected]

[email protected]

Bhavna Rote

11

[email protected]

drchiragpateld I [email protected]

Rammurthy Kulkarni

Chinmoy Roy

[email protected]

pbm_ I I/@yahoo.co.in

Chirag Patel

10

rep/[email protected]

[email protected]

Palak Mehta

Kinsuk Das kinsukl [email protected]

[email protected]

R Gurumoorthi

Chapter

Ayanangshu Nayak

16

[email protected]

8

Pankaj Surange [email protected]

17

Preface to the Second Edition

I

n the beginning, we wish to thank all of you for such an overwhelming response for the first edition whose copies were finished in just one and half years. All of you must be aware of the fact that this is the first book on clinical methods in pain medicine for a systematic approach in examining a patient with complaints of pain; and is the only book on pain medicine which focuses on evaluation and examination along with an easy to learn, evidence-based algorithm for the diagnosis. The effort was well appreciated across the world as it is being evident for the requirement of the second edition in less than 2 years. In this edition we have improved certain chapters, for example, introduction and history taking; and also you will be able to find a completely rewritten chapter on back pain. Along with this, we have also done our sincere efforts to take care of the minor mistakes which were there in the earlier edition. Hope all of you are going to appreciate our efforts and going to learn and spread knowledge about pain medicine everywhere.

Gautam Das

Preface to the First Edition

B

asic methods of evaluation of a patient have similar steps among different medical specialties, but each specialty has its own systematic approach. Pain medicine, considered as a different specialty, cannot be an exception. At present, there is a lack of uniformity and confusion among physicians about clinical methods in pain medicine. In practice, no patient will tell that 'I am suffering from neuropathic pain of fibromyalgia', so the doctor can prescribe pregabalin; nor patient will say that 'I am feeling pain of facet joint', so doctor can inject at facet joint. A physician must evaluate the patient to diagnose it as fibromyalgia or osteoarthritis of facet joint, to prescribe medicines or do interventions. As a pain physician, we need a good knowledge of orthopedician, neurologist, rheumatologist, physiatrist, psychiatrist with the skill of anesthesiologist, and neurosurgeon. During my classes I have always felt the need of a textbook which covers a systematic approach for evaluation of patients of pain. The methods need to have strong scientific foundations too, based on publications and evidence. My 15 years of clinical practice of pain medicine helped me to develop some systematic methods. This book is the arrangement of those approaches refined and extended further by my colleagues. Pain physicians around the whole world were in desperate need of such a book with sufficient photographs and illustrations. Physicians of other specialties will also be helped when they evaluate a patient suffering from pain. Our efforts will be successful if the physicians are benefitted by this book which is the first book of clinical method of this specialty. The following lines should be printed at the bottom of 'Preface to Volume 2' as has been done in the 1st volume of the book. 'The author appreciates the services and active support received from his following students during the course of the preparation of the manuscript of this volume'. Dr Ratna Chattopadhyay Dr Sourendra Kanta Goswami Dr Sanghamitra Ghosh Dr Radhika L Kundula

Gautam Das

Acknowledgements

I

am greatly helped by my junior colleagues in preparing this book. The fellows of Daradia Pain Clinic, namely Bhavna Rote, Rammurthy Kulkarni, Tarun Kumar Reddy, Chirag Patel and Mamta Mishra have not only contributed chapters but also helped in editing and taken photographs themselves. For 2nd edition, Kanchan Sharma and R Gurumoorthi helped a lot. I am thankful to my co-editors, Chinmoy Roy, Palak Mehta, R Gurumoorthi, and Samarjit Dey, for their contribution. They too have written some chapters and helped in editing the text, R Gurumoorthi in particular. I am thankful to whole editorial board who enriched the book with valuable editing. I am really grateful to CBS Publishers & Distributors Pvt. Ltd., for accepting to publish this book in a very short time, particularly Mr RN Mandal and Mr YN Arjuna.

Gautam Das

Contents Editorial Board and Co-Editors

ii

Contributors Preface to the Second Edition

vii ix

Preface to the First Edition

xi

1. Introduction to Clinical Methods in Pain Medicine

1

Gautam Das, Kanchan Sharma

2. History Taking in Pain Medicine

4

R Gurumoorthi, Gautam Das, Palak Mehta

3. General Examination in Pain Medicine

18

Chirag Patel, Rammurthy Kulkarni

4. Evaluation of Headache

23

Bhavna Rote

5. Evaluation of Neck Pain

38

Bhavna Rote, Mamta Mishra

6. Evaluation of Shoulder Pain

50

Tarun Kumar Reddy, Rammurthy Kulkarni

7. Evaluation of Hand Pain

63

Chirag Patel

8. Evaluation of Chest Pain

76

Samarjit Dey

9. Evaluation of Upper and Mid-Back Pain

89

Rammurthy Kulkarni, Tarun Kumar Reddy

10. Evaluation of Abdominal Pain R Gurumoorthi, Kinsuk Das

100

Clinical Methods in Pain Medicine

xiv

11. Evaluation of Low Back Pain

113

Kanchan Sharma, Chinmoy Roy, Karthic Babu N

12. Evaluation of Leg Pain

129

Chirag Patel, Mirghani Ali

13. Evaluation of Knee Pain

148

Sourav lswarari, Aniketa Banerjee, Saikat Majumdar

14. Evaluation of Joint Pain

161

Sourav lswarari, Dibyendu Das

15. Evaluation of Widespread Pain

170

Tarun Kumar Reddy, Rammurthy Kulkarni

16. Psychological Evaluation

181

Ayanangshu Nayak

17. Common Investigations in Pain Medicine

186

Pankaj Surange

Index

219

Chapter

1 Introduction to Clinical Methods in Pain Medicine Gautam Das, Kanchan Sharma

EACH SPECIALTY HAS ITS OWN DISTINCT CLINICAL METHODS

PAIN MEDICINE AIMS IN RELIEVING (CHRONIC) PAIN

Basic methods for clinical examination are similar among different medical specialties but each specialty has its own distinct approach for evaluation and management of the patient. For example, a chest physician after taking a history, examines the patient in the sequence of inspection, palpation, percussion and auscultation; an or thopedician has the sequence of inspection, palpation, range of motion. Pain medicine, if considered as a specialty should also have its own clinical methods for evaluation and management of a patient. Multidisciplinary mode of management is the basis for all the treatment plans in all the specialties but this mode of management is very much required in pain medicine. In pain medicine, more emphasis is being paid for on detailed history taking and clinical examination of the patient. The present scenario there is a lack of uniformity among the pain physicians in evaluating a patient. There is always a confusion, as how to proceed towards taking a history, what is its importance in pain medicine, and which system they should start examining first, what exactly is the sequence in which they are supposed to proceed further. Many questions like this are still unanswered. This is the reason behind the birth of this book so that we can have the uniformity in our clinical methods while evaluating a patient.

Since the inception of this branch pain physician's primary aim was to relieve pain. For that, their focus was to find out the best and long-term pain relief treatment plan in whatsoever may be the diagnosis and pathology behind it and whatsoever ways they have evaluated the patient. The problem starts here because if we miss the diagnosis, we might not be able to give long-term or permanent pain relief and at times we may miss a dangerous diagnosis too. As a pain physician, we need to have a good knowledge of orthopedics, neurology, rheumatology, physical medicine, and psychiatry and the skills of anesthesiologist and neurosurgeon. Let us start with a very common example. A patient consulted a pain physician with complaints of low back, buttock and thigh pain on right side. The physcian examined meticulously and suspected sacroiliac joint as the pain generator. He gave sacroiliac joint injection with local anesthetic and deposteroid and patient's pain was relieved within a few days. After a month, patient had developed similar pain on the left side. Physician again had gone for left-sided sacroiliac joint injection and patient had the same amount of relief. After sometime, right pain returned back with a new pain in the cervical region and mid- back. This time the patient had consulted a rheumatologist and he diagnosed it to be ankylosing spondylitis. Though the physician had nicely located the 1

2

Clinical Methods in Pain Medicine

pain generator and had done, the evidencebased interventional treatment also, but had missed the most probable pathology behind it. There are many such real life examples which make us realise that diagnosing the underlying pathology as pain generator, is equally important so as the intervention. Diagnostic intervention plays an important role in identifying a localized pain generator but it has got no role in identifying a systemic pathology like fibromyalgia. Difficulties are also encountered when we are dealing with chronic pain, because at times it is considered as a disease itself, where there is no specific sign, classical example is fibromyalgia. Pain is never a normal phenomenon; there is always a reason behind it which at times we would not be able to detect by clinical examination and recommended investigations. Detail history along with the proper assessment of pain generators give us various clues which helps in making a relevant diagnosis and formulating our pain relieving plans. History plays an important role in making a diagnosis. Here is an example for it, diagnosis of neuropathic pain is mostly by history, anticonvulsants and antidepressants drugs are the treatment modality. In other words, if we can arrive at a particular diagnosis, only then we can formulate the best treatment plan. For example, disc prolapse with radiculopathy, without red flag signs, we can explain the duration of conservative management and if failed, then appropriate interventions according to the hydration and the location of the disc prolapse. PAIN IS AN EVOLVING SPECIALTY, SCENARIO SHOULD BE CHANGED

Pain management is an evolving branch and there is no uniformity in the clinical methods for evaluation of a patient. The present scenario needs to be changed and more emphasis should be laid down in making our clinical methods uniform throughout the world. Three things to be kept in our mind

when we are evaluating a patient suffering from pain: First, detailed assessment of pain that includes the psychological aspect too. Second, to find out the pain generators as it can be one or multiple. Third, what exactly is the reason behind the pathology which has converted a normal tissue into a pain generator. How to make a diagnosis? The answer lies in the fact that there is a combination of the following four steps, 1 which helps us in making a diagnosis. They are detailed history and analysis of the symptoms, 2nd step-physical examination, 3rd step-different investigations, and 4th step-diagnostic intervention or diagnostic nerve block. In pain medicine, the first and fourth steps are very much important, which is slightly different from clinical methods of other specialties. Different models are there for the management of diseases like preventive care model where the aim is prevent the diseases from emerging. Curative care model, where aim is to cure the diseases based on diagnosis, and palliative care model where aim is palliation of symptoms alone.2 This model is appropriate when there is no cure for a particular disease like in malignancies3 and degenerative condition. MODEL OF 'DIAGNOSIS BASED CARE'

Pain medicine was initially started as a symptom palliation4 only. If we look back, initially pain physicians used to treat pain of patients who were suffering from incurable diseases, like malignancy. Then the era of multidisciplinary approach came, where physicians used to treat diseases and pain was being treated by the pain physicians. But over a period of time evolution has taken place, now we are in an era where pain physicians are not only involved in the symptom palliation, or in the treatment of pain arising from incurable diseases but are independently treating the curative diseases as well as performing the advanced procedures like percutaneous dissectomy. That is why, our

Introduction to Clinical Methods in Pain Medicine

approach to evaluate a patient needs to be changed. We need to change our model from palliation to cure now. We can make it possible only when we develop reasonable clinical skill in order to make a clinical diagnosis and able to locate the pain generators quite well. Depending on the situation it can be curative and palliative. This laid the foundation of the diagnosis based care model. In diagnosis based care model, if the diagnosis is curative, then we should make curative plans, but at the same time, attention needs to be paid towards pain palliation to. In case our diagnosis happens to be wrong, in other words supposedly the cure of the disease is not possible, we can just go with the palliation of the symptoms. This model makes us flexible in our approach while evaluating a patient. CLINICIAN IS A DETECTIVE OR INVESTIGATOR

As most of the pain generators are from musculoskeletal system, so we should have a good clinical knowledge about this system in order to be a good pain physician. Whenever a patient comes to us with complaints of pain in a particular region, we should think about all the structures present in that particular region and at the same time we should also think about the referred pain in that area from other areas. After ruling out the red flags, we should think about the common causes of pain followed by the less common and the rarest. Positive as well as negative clues from the history, clinical examination, investigations needs to be analyzed properly.

3

It is always the findings from the clinical examination, which is more important than any investigations when both of them happens to be contradictory. With the present scenario of medicolegal litigation, it is mandatory to write down the working diagnosis on outpatient prescription. Whenever we are not formulating a treatment plan based on our diagnostic model, we may end up giving the wrong treatment to the patient. Whenever we in a confusion in locating the pain generators where clinical findings and investigations are contradictory, it is always better to seek help from the other specialty person. In this book an effort has been made to discuss certain common conditions in pain and how to arrive to a particular diagnosis based on history, clinical examination which includes general and systemic, and relevant investigations.

I REFERENCES 1. Gurumoorthi R, Das G, Gupta M, et al. The art of history taking in patient with pain: An ignored but very important component in making diagnosis. Ind J Pain 2013; 27(2): 59-66. 2. Das G, Gurumoorthi R. Evolution of pain clinics. In: Das G, Roy C, Mehta P (Eds). How to start and run a pain clinic: including administration, finance and marketing? New Delhi. Wiley: 2014; p. 3-13. 3. Crawford GB, Price SD. Team working: Palliative care as a model of interdisciplinary practice. MJA 2003; 179: S32-4. 4. Meldrum ML. A Capsule History of Pain Management. JAMA 2003; 290: 2470-5.

Chapter

2

History Taking in Pain Medicine R Gurumoorihi, Gautam Das, Palak Mehta

also from experienced pain physicians who can narrate us their own experiences to us. History is also very important in ruling out the red flags which need more invasive management and treatment. For example, history of bladder and bowel dysfunction, weakness of legs, increasing numbness, history of malignancy and history of trauma in low back pain and leg pain, all point towards the red flags for low back pain. History taking can be divided into the following headings: • Pain at different locations as chief presenting complains • Ruling out red flags or warning signals • Past history • Psychological assessment • Personal history including sleep, bladder/ bowel habit • Treatment history • Family history. During history taking, we must remember the following: • Sufficient time must be given to the patients to express their complaints and what made them seek advice from the physician. • We need to listen carefully to the patients without any distractions in order to interpret the clinical information provided by them. • Physician should be empathetic. • Patient should believe that his/her physician is accepting his/her complaint. • The patient should be instructed to explain the history in chronological order. We

INTRODUCTION

Making a diagnosis based on patients complains is the keystone in laying down the foundation of treatment plans. The correct treatment plan targets the right pain generator and the pathophysiology behind it. In todays era, we are more dependent on the investigations and imaging modalities rather than in taking a detailed history and depending on our clinical skills. We rely on the MRI report rather than correlating it with the symptoms and clinical examination of the patient. History, clinical examination and investigations are the three keystone in making a clinical diagnosis. Diagnostic intervention or diagnostic nerve block which is a part of investigation plays an important role in locating the pain generators. We can depend on it rather than depending on sophisticated non-investigations modalities in locating the pain generators. Importance should always be given to detail history taking because it really helps in locating the pain generators and it avoids unnecessary investigations at the same time. Special attention needs to be given to anxious, depressed or overtly frightened, patients who over a period of time have started feeling hopeless regarding the treatment of their pain. Repeated history taking from various patients with chronic pain can help us in gaining the experience in making a diagnosis and to handle the situation better which may be confusing initially. It is an art which we can learn from the standard textbooks as well as 4

History Taking in Pain Medicine

should not intervene in between when the patient is expressing it, but at the same time we can ask questions in between in case we feel some portion of it to be irrelevant. • Assess what exactly is the effect of pain on their psychological, socioeconomic, and spiritual life. Detailed history should be taken on the first visit. It is going to be time-consuming and laborious. Pre-consultation questionnaire can play a very important role in solving this issue. They can be used for baseline reference for any kind of pain. While taking the detail history focuse should be on the type of pain and the reason behind it. We should start taking history, with a simple introduction about the patient itself, which includes age, education, job, living place, spouse and kids, education, professional life and social environment. Pain history consists of the following

• • • • • • • • •

Quantity or severity of pain. Quality or nature of pain. Mode of onset and location. Duration or chronicity. Provocative and relieving factors. Special character. Timing of pain. Relation to posture. Associated complaints

Some clinicians prefer the mnemonic 'SOCRATES' but it is up to the readers to understand the importance and impact of each subheading in making a diagnosis. Quantity or Severity or Intensity of Pain

Pain is a subjective experience. Like many diseases such as hypertension or diabetes, there is no objective measurement for a patient's pain intensity. Unfortunately, we do not have a thermometer like device to measure pain so we need to rely on the patient's statement. Pain is complex neurobehavioral problem affected by psychological, cultural, and environmental factors. The variables to be measured are current pain intensity and

5

average pain intensity over a specified period of time, e.g. last 1 week or 4 weeks. It is the average pain intensity which is the usual target for pain treatment, both by the clinician and the patient. The goal of treatment in acute or chronic pain is to reduce pain intensity as much as possible while avoiding side effects and to increase the acceptance of the present line of treatment. Numerous pain scales for practical assessment of pain intensity in clinical studies have been developed. The chosen one should be appropriate to the patient's abilities and preferences. These scales are more appropriate for detecting changes within individuals rather than comparison between individuals and also help in assessing the response to treatment. Types of Pain Intensity Assessment

Pain can be assessed in two ways, either by unidimensional or multidimensional instruments. We should assess patient's pain with movement not when he/she is lying comfortably in bed. Unidimensional Instruments

• Verbal rating scales (VRS): In VRS, pain is described as none, mild, moderate, or severe. This is the usual way a patient expresses pain. This scale is short, easy to use and understand, especially in elderly and illiterate. Patient's lack of reproducibility makes this one less suitable for research purposes.1 • The binary scale: The patient is asked to

answer questions like-Do you have a 60% relieve in your pain? "Yes or No". This is short, easy to use and understand. Sometimes patient himself/herself is expressed in this way which can be misleading along with this lack of reproducibility make this less suitable for research purposes. • The numerical rating scale (NRS): It is most commonly used. In this the two extreme experiences of the pain is noted and has a numerical scale between "no pain" and "worst pain imaginable". "Zero" corresponds to no

6

Clinical Methods in Pain Medicine

pain and "10" corresponds to the worst pain imaginable (Fig. 2.1). It is easy to understand but the disadvantage is that the digital scale reduces the capacity to detect subtle changes as the digits act as anchoring points. A reduction of 30% or 2 points and more from baseline in patient's on treatment indicate a positive response for treatment. • The faces rating scale: It is commonly used. The patient is asked to point at various facial expressions ranging from a smiling face (no pain) to an extremely unhappy one (the worst possible pain). It is used when the communication with the patient is difficult as with the pediatric and deaf and dumb patients. • The visual analog scale (VAS): It is similar to

the numerical rating scale. There is a 10 cm horizontal line with a label of "no pain" at one end and "worst pain imaginable" at the other end. The patient is asked to mark on this line where he feels the intensity of his/her pain lies. The distance from "no pain" to this mark indicates the severity of pain numerically. Slide rule-like devices are also available that make measurement easier. The device has a line on the patient side and a numeric score on the clinician side. The VAS is a simple, efficient, valid and minimally intrusive method that correlates well with other reliable methods. The disadvantage is that it is more time-consuming than other instruments. There is some difficulty in using and understanding this scale in elderly patients. No pain 0

Multidimensional Instruments

• The McGill pain questionnaire (MPQ) :2, 3 It was developed by Melzack and Torgerson. It is a checklist of words describing symptoms. Unlike other scales, it attempts to define the pain in 3 major dimensions by 20 sets of descriptive words divided as: a. 10 sets describe sensory-discriminative (nociceptive pathway). b. 5 sets describe motivational-affective (reticular and limbic structures). c. 1 set describes cognitive-evaluative (cerebral cortex). d. 4 sets describe miscellaneous dimensions. The patient selects the sets that apply to his or her pain, and circles the words in each set that best describe the pain. The words in each class are given a rank according to severity of pain. It is translated into multiple languages. The advantage is that it is reliable and can be completed in 5-15 minutes and it helps in the diagnosis as the choice of descriptive words that characterize the pain correlates well with pain syndromes. The disadvantage is that high levels of anxiety and psychological disturbance can obscure the MPQ's discriminative capacity. It was also too long and omission of pain history and interference with activities. • Brief pain inventory (BPI) :4 It measures both the intensity of pain (sensory dimension) and its interference the patient's life (reactive dimension). People have translated it into multiple languages. We can use it for disabled people too. Advantages a. It is reliable and valid for cancer pain and various pain syndromes.

Moderate pain

2

3

4

5

6

Excruciating pain

8

7

9

10

I=I=I=I=I=I=I=I=I=I=I Mild pain

Severe pain

Fig. 2.1 Numerical rating scale

History Taking in Pain Medicine

b. Easy to complete in 5-1 minutes. c. It shows good sensitivity to treatment (mostly in pharmacological treatments). d. Helps in comparing international trials with different culture and population. e. First choice of multidimensional pain scale in clinical setting and research activities. • West Haven-Yale multidimensional pain inventory (WHYMPI)5, 6

Technique: It is composed of 52 items with 3 parts: Part I: 20 questions to assess the five pains related domains which includes interference, support, pain severity, self-control and negative moods. Part II: Assess the spouse response to patient pain behavior.

Part III: Participation in various life activities. Patient's response to question is noted on a 7-point scale.

Advantages a. It is valid in many pain syndromes. b. It shows good sensitivity to treatment effects. • Medical outcome study 36-item short-form (SF-36) health survey:7' 8 It is commonly used in health economics. It consists of 8 subscales including: 1. Physical functioning. 2. Limitations due to physical problems. 3. Social functioning. 4. Bodily pain. 5. Role limitations due to emotional problems. 6. General mental health. 7. Vitality. 8. General health perceptions.

Advantages a. It is the most widely used instrument to measure multiple dimensions of quality of life. b. It is used in almost every disease or conditions imaginable.

7

c. It is easy to administer, taking about 10 minutes to complete.

Disadvantages a. No addition to sleep profile b. Low response to patient with age above 65 years. Assessment of Quality or Nature of Pain It is one of the most important components in making a diagnosis, particularly if we want to diagnose the nature or character of pain whether it is nociceptive or neuropathic or a mixed nature. There are different validated questionnaires based tools which help us in identifying neuropathic pain conditions. And most of these tools are based on analysis of history. Even when we are not using such tools, proper history can guide us in making diagnosis of neuropathic pain. Simple questions like whether there is burning sensations, tingling, numbness, sensations like crawling of ants, cramping, electric shock-like pain, etc. can guide us to understand whether there is neuropathic component of pain is present or not. Allodynia can also be assessed by history, when clothes touching body parts are simple touch with fingers is causing pain. Nociceptive pain is somewhat easily manageable. Neuropathic pain if not diagnosed properly within a time period and treated properly can lead to the catastrophic stage which is not amenable to treatment modalities. Neuropathic pain has been defined by NeuPSIG (Special Interest Group on Neuropathic Pain), a "pain arising as a direct consequence of a lesion or disease affecting the somatosensory system".9 It is a common type of pain associated with suffering, depression, anxiety, disturbed sleep and impaired quality of life. Since these components require different pain management strategies, correct diagnosis is highly desirable.l" Presence of validated tools to diagnose neuropathic pain is therefore required as improper assessment is frequently associated with under treatment, under diagnosis and increased cost to the

Clinical Methods in Pain Medicine

8

patient and society as a whole. A number of screening tools in the form of questionnaires have been developed and validated in the past decade to solve the above problem. Screening Tools for Neuropathic Pain

• Leeds assessment of neuropathic symptoms and signs (LANSS): LANSS, first described in 2001,11 was the first screening test to identify the pain of neuropathic origin. It is a simple tool with two components. First is a questionnaire which consists of 5 symptoms addressing pain quality and triggers and second is sensory testing which consists of 2 signs (Table 2.1). Each item is a binary response (yes or no) to the presence of symptoms (5 items) or clinical signs (2 items). It is easy to score in clinical settings and has been tested and validated in a number of neuropathic pain conditions with a sensitivity and specificity ranging from 82 to 91 % and 80 to 94% respectively.12-15 Table 2.1: Leeds assessment of neuropathic symptoms and signs (LANSS)16 [Scores in bracket]

Symptoms

Signs

Pricking, tingling, pins and needles sensation [5]

Brush allodynia [5]

Electric shocks or shooting [2] Raised pinprick threshold [3] Skin color change [5] Pain evoked by light touch [3] Skin temperature like hot or burning [1]

Score 40-extreme depression Hamilton depression scale It includes 17 parameters with score grade of 0 to 4 (symptom is absent, mild, moderate or severe) thus total score of 54.

12

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Clinical Methods in Pain Medicine

PHQ-9 Not at all

Several days, but less than half a month

Several days, more than half a month

Nearly everyday

A. A little interest or pleasure in doing things

0

1

2

3

B. Feeling down, depressed or hopeless

0

1

2

3

C. Trouble falling or staying asleep or sleeping too much

0

1

2

3

D. Feeling tired or having a little energy

0

1

2

3

E. Poor appetite or overeating

0

1

2

3

F. Feeling bad about yourself or that you are a failure or 0 have let yourself or your family down

1

2

3

G. Trouble concentrating on things such as reading the newspaper or watching television

0

1

2

3

H. Moving or speaking so slowly or so restlessly that other people could have noticed

0

1

2

3

I. Thoughts that you would be better off dead, or thoughts of hurting yourself in some way

0

1

2

3

Maximum score is 27. Score 1-4/27 indicates minimal depression, 5-9/27 indicates mild depression, 10-14/ 27 indicates moderate depression, 15-19 /27 indicates moderately severe depression and 20-27 /27 indicates severe depression.

Zung self-rating depression score It includes 20 parameters with grading ranging from 1 to 4 thus total score of 20-80. Some parameters are given score from 1 to 4 for symptoms increasing in time duration and some are given in reverse. Hospital anxiety and depression scale (HADS)

It includes 14 parameters with 2, 4, 6, 8, 11, 12, 14 for anxiety and 1, 3, 5, 7, 9, 10, 13 for depression. Scoring is done as 3, 2, 1, 0 (for item 7 and 10 scoring is reversed). A score of 0-7 indicates non-case; 8-10 indicates borderline case and 11 or above indicates case. Pain catastrophizing scale (PCS) and the Tampa

scale of kinesophobia helps in assessing personality disorder.

Personal History Including Sleep, Bladder/ Bowel Habit

Sleep disorder and pain is highly interlinked. Pain can cause sleep disorder in over 70% of patients. Pain may be interrupted, e.g. posttraumatic stress disorder or patient cannot feel fresh on waking up, e.g. in fibromyalgia. Some disorders associated with sleep like obstructive sleep apnea can interfere with treatment and result, e.g. treatment with opioids. Effective treatment of sleep disturbance involves assessing and treating all of the contributing factors. Pregnancy should be ruled out in women of childbearing age. Bladder and bowel disturbance may be an associated component or etiology for present pain complaint. For example, history of inflammatory bowel disease may be reason for seronegative inflammatory arthropathy and irritable bowel disease may be an associated disease for fibromyalgia.

History Taking in Pain Medicine

13

Treatment History

Family History

The initial questionnaire should allow the patient to list all the therapeutic modalities they are currently using or have used in the past. Chances of drug addiction should be ruled out before prescribing any drugs. Any drug allergy, any side effect/ complication of past treatment or co-morbid condition (renal, hepatic compromise) should be taken into account before prescribing medicine.

History of pain and disease among the family members can help us in making a diagnosis because some diseases run among families, e.g. rheumatoid arthritis and fibromyalgia. History of family dispute should be ruled out in patients having disproportionate, irrelevant and unusual manifestation.

Sample History Sheet Personal details 1. Name:

Date:

2. Age:

Sex:

3. Address: .

..

..

..

..

..

. Religion:

.. . ..

..

..

..

..

Occupation: ..

.. ..

. .

4. Marital status (Single/ Married/ Separated/ Other): Detailed history of pain 5. Mode of onset of pain (sudden or gradual): 6. Quantity or severity of pain:

.

(Grade it as per following numerical rating scale beside questions below a, b and c)

Numerical rating scale (NRS) No pain

0

Moderate pain 1

2

3

4

5

6

Excruciating pain

7

8

9

10

l=l=l=l=l=l=l=l=l=l=l Mild pain

a.

Severe pain

How is your pain now, at this moment?

b. How strong was the strongest pain during the past one month? c.

How was your average pain during the past one month?

7. Duration of pain (in days/months/years)

Contd ...

Clinical Methods in Pain Medicine

14

8. Location: Mark area of pain in the picture below:

9. Quality or nature of pain: Burning sensation/tingling/pricking of needles sensation/sensation like crawling of ants/pain with light touch/ sudden electric shock like pain/itching/ cramping/pain on application of cold or heat/ numbness/pain on slight pressure/stabbing pain/radiation of pain 10. Does your pain radiate/spread from one part to other parts? Yes/No 11. Pain in relation with posture (mark whether your pain increases or decreases or no changes with following postures): a. Sitting (increases/ decreases/no changes) b. Lying down (increases/decreases/no changes) c. Standing (increases/ decreases/no changes) d. Bending forward (increases/decreases/no changes) e. Chage of posture from sitting to standing (increases/ decreases/no changes) f. Walking (increases/decreases/no changes) g. Lifting something (increases/ decreases/ no changes) 12. Pain provocating factors 13. Pain relieving factors 14. Timing of pain (morning/ evening/ any time after rest/ anytime after work) 15. Associated complaints with pain (e.g. fever, vomiting and headache) Contd ...

15

History Taking in Pain Medicine

History of Mental Health 16. Psychological assessment: By PHQ-9 to detect depression (the below chart is reproduced with permission from Pfizer Inc.) (Ref: Kroenke K, Spitzer RL, Williams JBW. The PHQ-9: Validity of a brief depression severity measure. J Gen Intern Med 2001;16:606-13) Not at all

Several days, but less than half a month

Several days, but more than half a month

Nearly everyday

A.

A little interest or pleasure in doing things

0

1

2

3

B.

Feeling down, depressed or hopeless

0

1

2

3

C.

Trouble falling or staying asleep or sleeping too much

0

1

2

3

D.

Feeling tired or having a little energy

0

1

2

3

E.

Poor appetite or overeating

0

1

2

3

F.

Feeling bad about yourself or that you are a failure or have let yourself or your family down

0

1

2

3

G.

Trouble concentrating on things such as reading the newspaper or watching television

0

1

2

3

H.

Moving or speaking so slowly or so restlessly that other people could have noticed

0

1

2

3

I.

Thoughts that you would be better off dead, or thoughts of hurting yourself in some way

0

1

2

3

Interpretation: 1-4 Minimal depression, 5-9 Mild depression, 10-14 Moderate depression, 15-19 Moderately severe depression, 20-27 Severe depression

Medical History 17. Did you have any injuries? lfyes, please describe it. 18. What are the medicines that you have taken to reduce pain? 19. How much relief are you getting from these medicines? (Not at all/Partial/Good/Excellent) 20. Are you suffering from other diseases? (For example diabetes mellitus, hypertension and hypothyroidism) 21. Did you have any operations earlier? If yes, please describe it. Family and Personal History 22. Do your 1st degree relatives suffer from any painful conditions? 23. Describe your sleep pattern. 24. History of alcohol/drug intake. 25. Bladder and bowel habit.

16

Clinical Methods in Pain Medicine

I REFERENCES 1. Williamson A, Hoggart B. Pain: A review of three commonly used pain rating scales. J Clin Nurs 2005;14:798-804. 2. Melzack R. The McGill Pain Questionnaire: Major properties and scoring methods. Pain 1975;1:277-99. 3. Melzack R. The Short-Form McGill Pain Questionnaire. Pain 1987;30:191-7. 4. Cleeland CS, Ryan KM. Pain assessment: Global use of the brief pain inventory. Ann Acad Med Singapore 1994;23:129-38. 5. Dworkin RH, Turk DC, Farrar JT, et al. Core outcome measures for chronic pain clinical trials: IMMPACT recommendations. Pain 2005; 113:9-19. 6. Kerns RD, Turk DC, Rudy TE. The West Haven-Yale Multidimensional Pain Inventory (WHYMPI). Pain 1985;23:345-56. 7. Ware JE, Sherbourne CD. The MOS 36-item Short-Form Health Survey (SF-36), I: Conceptual framework and item selection. Med Care 1992;30:473-83. 8. Kazis LE, Miller DR, Clark J, et al. Health related quality of life in patients served by the Department of Veterans Affairs: Results from the Veterans Health Study. Arch Intern Med 1998;158:626-32. 9. Treede RD, Jensen TS, Campbell JN, et al. Redefinition of neuropathic pain and a grading system for clinical use: Consensus statement on clinical and research diagnostic criteria. Neurology 2008;70:1630-5. 10. Freynhagen R, Baron R, Gockel U, et al. pain DETECT: A new screening questionnaire to detect neuropathic components in patients with back pain. Curr Med Res Opin 2006;22: 1911-20.

13. Yucel A, Senocak M, Kocasoy Orhan E, et al. Results of the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale in Turkey: A validation study. J Pain 2004;5: 427-32. 14. Khedr EM, Koth H, Kamel NF, et al. Longlasting analgesic effects of daily sessions of repetitive transcranial magnetic stimulation in central and peripheral neuropathic pain. J Neurol Neurosurg Psychiatry 2005;76: 833-8. 15. Kaki AM, El-Yaski AZ, Youseif E. Identifying neuropathic pain among patients with chronic low back pain: Use of the Leeds Assessment of Neuropathic Symptoms and Signs Pain Scale. Reg Anesth Pain Med 2005;30:422-8. 16. Bennett Ml, Smith BH, Torrance N, et al. The S-LANSS score for identifying pain of predominantly neuropathic origin: Validation for use in clinical and postal research. J Pain 2005;6: 149-58. 17. Krause SJ, Backonja MM. Development of a Neuropathic Pain Questionnaire. Clin J Pain 2003;19:306-14. 18. Backonja MM, Krause SJ. Neuropathic Pain Questionnaire-short-form. Clin J Pain 2003; 19:315-6. 19. Bouhassira D, Attal N, Alchaar H, et al. Comparison of pain syndromes associated with nervous or soma tic lesions and development of a new neuropathic pain diagnostic questionnaire (DN4). Pain 2005; 114:29-36. 20. Freynhagen R, Tolle TR, Baron R. pain DETECT-ein Palmtop basiertes verfahren fur versorgungsforschung, Qualitatsmanagement und screening bei chronischen Schmerzen. Akt Neurol 2005;34:641.

11. Bennett Ml. The LANSS Pain Scale: The Leeds assessment of neuropathic symptoms and signs. Pain 2001; 92: 147-57.

21. Freynhagen R, Baron R, Gockel U, et al. pain DETECT: A new screening questionnaire to detect neuropathic components in patients with back pain. Curr Med Res Opin 2006;22: 1911-20.

12. Potter J, Higginson IJ, Scadding JW, et al. Identifying neuropathic pain in patients with head and neck cancer: Use of the Leeds Assessment of Neuropathic Symptoms and Signs Scale.JR Soc Med 2003;96:379-83.

22. Bouhassira D, Attal N. Diagnosis and assessment of neuropathic pain: The saga of clinical tools. Pain 2011;152:S74-83. 23. Portenoy R. For the ID Pain Steering Committee. Development and testing of a neuropathic pain

History Taking in Pain Medicine

17

screening questionnaire: ID-Pain. Curr Med Res Opin 2006;22:1555-65.

study. Int J Clin Health Psychol 2009;9: 143-59.

24. McCaffery M, Beebe A. Pain: Clinical Manual for Nursing Practice. Baltimore: V.V. Mosby Company; 1993.

27. Bjelland I, Dahl AA, Haug TT, et al. The validity of the hospital anxiety and depression scale, an updated literature review. J Psychosom Res 2002; 52: 69-77.

25. Cusin C, Yang H. Rating scales for depression. In: Baer L, Blais MA (Eds). Handbook of Clinical Rating Scales and Assessment in Psychiatry and Mental Health. New York: Humana Press; 2010. 26. Lopez-Pina JA, Sanchez-Meca J, Risa-Alcazar Al. The Hamilton rating scale for depression: A meta-analytic reliability generalisation

28. Sullivan MJ. The Pain Catastrophizing Scale User Manual. Montreal, 2009. 29. Burwinkle T, Robinson JP, Turk DC. Fear of movement: Factor structure of the Tampa Scale of Kinesophobia in patients with fibromyalgia syndrome. J Pain 2005; 6:384-91.

Chopter

3 General Examination in Pain Medicine Chirag Patel, Rammurthy Kulkarni

Depressed face: Apathy or blunt expression, flat affect, poor eye contact, associated with psychomotor slowing.

INTRODUCTION

General examination plays an important role when we are evaluating a patient suffering from pain. We can have better information regarding patients health and also help us in making a right clinical diagnosis. The primary aim of this chapter is to focus on the general examination part and its importance in making a right clinical diagnosis.

Moon face: A rounded moon face with red cheeks indicates Cushing's syndrome or longterm steroid therapy for painful conditions like inflammatory arthropathies. Face in myxedema: Dull puffy faces with nonpitting periorbital edema, hairs of the eyebrows are dry, coarse and loss of hair on outer third of the eyebrow. It is found in patients with hypothyroidism.

GENERAL OBSERVATIONS 1

The pain physician should observe the patient at a glance and look for: 1. Signs of distress 2. Facial appearance 3. Gait and posture 4. Mental state 5. Built and nutrition 6. State of clothing

Mask-like face: A mask-like face with decreased facial mobility and expressionless face is seen in Parkinsonism. Starring look: It is seen in depression as well as hyperthyroidism. Face in renal disorders: Periorbital edema with puffy eyelids in the morning, which makes the eyes look like slit is seen in patient's of nephrotic syndrome.

Signs of Distress

Look whether the patient is wincing, sweating and guarding painful areas. Clutching of chest, pallor, diaphoresis, labored breathing, etc. which may indicate respiratory or cardiac involvement.

Posture and Gait1

Posture and gait are quite informative for the examiner. Posture: Look at the posture which the patient has preferred to be comfortable. For example, leaning forward, stooped posture is the comfortable and preferred for patient with lumbar canal stenosis.

Facial Appearances2

Facial appearances will give many clues to the examiner. Anxious face: This kind of facial appearance is due to pain and anxiety. Patients usually have cold and sweaty palms.

Gait: Examples of various gaits and their clinical importance. 18

19

General Examination in Pain Medicine

Mental State Examination3

Speech

Look whether the patient is awake, alert and responsive to an examiner or surrounding. Simple and quick way to assess the mental state.

• Ask the patient to repeat two simple sentences, such as the following: - Today is a lovely day. - Ask the patient to name some objects which are there in the room? Ask the patient to rhyme simple words such as ball, pat and can.

Orientation

• Ask the following What is your full name? What is the year? Who is the president? Calculations

• Ask the following How many paisas in one rupee? Memory

• Ask the following questions Ask the patient three items to remember (examples: A red ball, a blue telephone, and address 66 Hill Street). Converse with the patient for sometime and ask the patient to repeat the list.

Comprehension

• Ask the patient to do the following Put the right hand on the left hand. Then ask the patient to point to the ceiling with the left index finger. Built and Nutrition

Look whether patient is well built, well nourished, or poorly built and poorly nourished. Poorly nourished or cachectic patients are seen in case of malignancy, tuberculosis, etc.

Gait

Features

Diseases

Antalgic gait

Limited range of motion with inability to bear full weight on affected extremity results in limp with slow and short steps. Staggering wide based gait, positive Romberg's sign. Hesitation on starting to walk and on turning. Weak and spastic limb extended and circumducted. Stiff scissor like walk with leg adduction and extension. Associated with bilateral weakness. Shuffling gait with short steps. Pelvis rotates >40° in axial plane towards the affected hip. Maladaptive gait allows for terminal hip extension on walking. Unsteady gait, worse with vision impairment or at night. Positive Romberg's sign Hyperflexed hips and knees on ambulation which compensates for foot drop. Pelvis tilts to the normal side while upper trunk tilt to the affected side. Swaying, symmetric, wide based gait with toe walking.

Degenerative arthritis, injury, fracture, septic arthritis.

Cerebellar gait Frontal gait (gait apraxia) Hemiparetic gait Paraparetic gait Parkinsonism gait Pelvic rotational wink

Ataxic gait Stepping gait Trendelenburg gait Waddling gait

Cerebellar CVA, vitamin 812 deficiency. Dementia, non-pressure hydrocephalus. CVA with hemiparesis. Spinal cord lesions, bilateral cerebral lesion. Parkinsonism. Intra-articular hip disorders.

Diabetic neuropathy, vitamin 812 deficiency. Distal motor neuropathy. Abductor weakness (gluteus medius) or intrinsic hip pathology. Osteitis pubis, pregnancy, muscular dystrophy.

20

Clinical Methods in Pain Medicine

State of Clothing

Respiratory Rate

For example, patients with hypothyroidism usually wear more clothes because of cold in tolerance.

The normal respiratory rate is 14-18/minute. Pain and anxiety can cause tachypnea.

IMPORTANT PARAMETERS IN GENERAL EXAMINATION2· 4

COMPLETE EXAMINATION FROM HEADTOTOE4 Head

Height, Weight and BMI

Always assess height, weight, and BMI • BMI = weight (kg)/height (m2). •Normal= 18-25 • Over weight ~30 • Obesity ~30 • Morbid obesity ~40 • Obesity predisposes to osteoarthritis. Check Vital Parameters Pulse

Check radial artery for rate, rhythm, character and volume. Bradycardia (pulse rate 100/min) is seen in anxiety, smoking, hyperthyroidism, drug induced and painful conditions. Also check femoral, popliteal, dorsalis pedis for peripheral vascular disease like Buerger's disease. Blood Pressure

Look for the size and shape of head. Look for anencephaly, microcephaly, macrocephaly (e.g. macrocephaly present in hydrocephalus, microcephaly in cerebral palsy). Hair

Look for hair loss. Hair loss may be present in a hypo- or hyperthyroidism, cancer patients on radiotherapy or chemotherapy. Eyes

Look for conjunctivitis, uveitis, iridocyclitis which may be present in inflammatory arthropathies like ankylosing spondylitis. Look for unilateral ptosis in Homer's syndrome and bilateral ptosis may be present in myasthenia gravis. Also look for exophthalmos which is present in hyperthyroidism. Oral Cavity

Examine the teeth, gums, lips, pharynx, tongue, and tonsils. Hypertrophic gums may be due to phenytoin therapy. Look for any painful ulcers, carcinomatous growth, tonsillitis, dental caries, etc.

Check for blood pressure with appropriate size cuff in the right arm in supine position. Also check standing blood pressure to rule out orthostatic hypotension (drugs like clonidine can cause orthostatic hypotension). Pain and anxiety usually cause high blood pressure.

Check for any discharge from the ear, running nose, etc. Palpate mastoid process, external ear as well as sinuses for any tenderness. For example, sinusitis and mastoiditis can cause headache or facial pain.

Temperature

Skin

Check oral or rectal temperature with a thermometer (e.g. increased temperature is suggestive of infection. Hypothyroidism can cause decrease temperature).

Look at skin for any changes. Following are the important skin lesions for pain physician. • Cyanosis which is seen in Raynaud's phenomenon, cyanotic heart diseases, etc.

Ear, Nose and Throat

21

General Examination in Pain Medicine

• Jaundice which is seen in hemolytic diseases, hepatobiliary diseases, etc. • Pyoderma gangrenosum which is seen in rheumatoid arthritis, ulcerative colitis, etc. • Eythema nodosum which is seen in tuberculosis, connective tissue disorders and poststreptococcal infections. • The butterfly rash (heliotropic) over the face and diffuse pigmentation which is seen in SLE. • Vesicular lesions along the dermatomal distribution which is seen in herpes zoster. Nail

Look for color and changes in nail. • Pale: Anemia • Yellow: Jaundice • Bluish: Cyanosis • Red: Palmar erythema • Petechial purpura: Bleeding or coagulation disorders. Clubbing

Due to increase in anteroposterior and transverse diameter of the nails, there is a bulbous enlargement in soft tissue of terminal phalanges producing transverse and longitudinal curving of nails. Common causes of clubbing • Cardiac: Cyanotic heart disease, subacute

bacterial endocarditis. • Respiratory: Bronchiectasis, lung abscess and bronchogenic carcinoma. • GIT: Ulcerative colitis and Crohn's disease (reactive arthritis). • Hepatobiliary: Biliary cirrhosis. Neck

Look for swelling or goiter in the neck. Palpate the enlarged lymph nodes. Lymphadenopathy is present in tuberculosis, metastatic carcinoma in supraclavicular region. Extremities2

Both upper and lower limb extremities can provide important information to examiner as follows.

Upper Extremity

Significant swellings in the hand Swelling

Significance

Heberden nodules (hard bony nodules in dorsum of hand in distal interphalangeal joints) Bouchards nodule (hard nodules on dorsum of proximal interphalangeal joints)

Osteoarthritis

Rheumatoid nodules

Rheumatoid arthritis

Osteoarthritis

Hand deformities • Swan-neck (hyperextended PIP and flexed DIP joints) and boutonnieres deformity (flexed PIP and hyperextended DIP joints) seen in rheumatoid arthritis. • Ulnar deviation of hand and Z deformity in rheumatoid arthritis. • Dupuytren's contracture (Hexion deformity of 4th and 5th fingers) • Trophic changes like ulceration, burns, etc. Lower Extremity • Foot drop: It is seen in sciatica or common

peroneal nerve palsy. • Joints: Arthritis may involve the small

joints of the foot in rheumatoid arthritis and psoriasis. Ankle joint may be involved in osteoarthritis. Painful swelling of joints of the big toes is seen in gout (podagra). Charcot joint which is seen in neuropathy, commonly involve the knee, hip, ankle producing painless huge swelling. • Trophic ulcers: Present in diabetic neuropathy, especially in pressure points like sacrum, heal and pad of the great toe. • Trophic changes in extremities: Trophic changes like increased hair or nail growth, contractures and fibrosis of skin, scaly epidermis (changes in skin and subcutaneous tissue) seen in patients of CRPS. Edema

Look for localized as well as generalized edema. Check whether pitting or nonpitting edema by applying firm pressure with thumb for at least 5-10 seconds at the ankle above

22

Clinical Methods in Pain Medicine

the medial malleolus, lower end of tibia and then release the pressure. Pit staying for >30 seconds is called pitting edema. The common causes of pitting and nonpitting edema are: • Pitting edema - Congestive heart failure - Constrictive pericarditis - Cirrhosis of liver - Nephrotic syndrome - Hypoproteinemia - Drugs like nifedipine/ amlodipine - Cushing' s syndrome - Steroid use • Nonpitting edema - Hypothyroidism. Fibromyalgia Tender Points

Look for tender points in patient with suspected fibromyalgia on both sides as below: • Occiput (suboccipital muscle insertions) • Trapezius (midpoint of the upper border) • Supraspinatus (medial border of the scapular spine) • Gluteal (upper outer quadrant of buttock)

• Greater trochanter • Low cervical (anterior aspect of the intertransverse process at CS-7) • Second rib (second costochondral junction) • Lateral epicondyle of elbow • Knee (medial fat pad proximal to the joint).5

I REFERENCES 1. Bickly LS, Szilaggyi PG. Bates guide to physical examination and history taking. Philadelphia: Lippincott Williams and Wilkins; 2002. 2. Colledge NR, Walker BR, Ralston SH (Eds). Davidson's Principles and Practice of Medicine. Edinburgh: Churchill Livingstone, Elsevier; 2010. 3. Waldman S. Physical Diagnosis of Pain. Philadelphia: Elsevier; 2005. 4. Chugh SN. Clinical Methods in Medicine (clinical skills and practices). New Delhi: Jaypee; 2011. 5. Wolfe F, Clauw DJ, Fitzcharles MA, et al. The American College of Rheumatology preliminary diagnostic criteria for fibromyalgia and measurement of symptom severity. Arthritis Care Res (Hoboken) 2010;62: 600-10.

Chapter

4

Evaluation of Headache Bhavna Rote

INTRODUCTION

Table 4.1: Pain sensitive structures of the head

Headache is one among the most common reasons patients seek medical attention.1 Patient having headache with or without facial pain experience severe discomfort and interference with daily routine activities, or raises the concern about serious underlying cause which may be responsible for visit to pain clinic. The gold standard for diagnosis and management of headache is a careful interview supported by neurological and general medical examinations (De Luca and Bartleson, 2010).2,3 (International Headache Society Classification Subcommittee, 2004.) International classification of headache disorders (ICHD) approach to classification defines three overarching categories: Primary headache disorders, secondary headache disorders and painful cranial neuropathies, other facial pains and other headaches.4 The primary headaches are those disorders that do not have underlying structural causes and secondary headaches are associated with some underlying structural causes. This classification is sometimes difficult to identify clinically as both may be present together. This can be diagnosed by meticulous history, neurological and general examinations, and appropriate investigations if needed2 and dual controlled diagnostic blocks. There are various structures, which can be the pain generators or source of pain for headache5 (Table 4.1). Recently International Headache Society had published ICHD, 3rd edition (beta

A. Extracranial • Scalp-skin, subcutaneous tissue, and periosteum of skull • Joints capsules-particularly the cervical and temporomandibular joints • Muscles-scalp and paraspinal muscles • Paranasal sinuses • Teeth • Ocular contents B. Intracranial • Blood vessels-arteries, veins and venous sinuses • Meninges-arachnoid, pia and dura mater • Cranial nerves

version) where headache was divided broadly into three categories which include primary headache, secondary headache and painful cranial neuropathies, other facial pains and other headaches (Tables 4.2 and 4.3). Each disease was given codes to simplify it and can be applied uniformly among different nations. In this chapter we have provided major classification and readers are requested to refer to the official page of international headache society for further details. Among all types of headache, the most common type of headache is a tension type headache among general population followed by migraine in primary headache though migraine is the most common type of headache among patient visiting pain clinic. Systemic infection induced headache is common among secondary headache disorders. The incidence of various headaches is given in Table 4.3. 23

Clinical Methods in Pain Medicine

24

Table 4.2: The headache classification (modified) (numbers refer to the ICHD-3 code)4·6·7

1. Migraine 1.1 1.2 1.3 1.4 1.5 1.6

Migraine without aura Migraine with aura Chronic migraine Complications of migraine Probable migraine Episodic syndromes that may be associated with migraine

2. Tension-type headache (TTH) 2.1 2.2 2.3 2.4

Infrequent episodic tension-type headache Frequent episodic tension-type headache Chronic tension-type headache Probable tension-type headache

3. Trigeminal autonomic cephalalgias (TA Cs) 3.1 Cluster headache 3.2 Paroxysmal hemicranias 3.3 Short-lasting unilateral neuralgiform headache attacks 3.4 Hemicrania continua 3.5 Probable trigeminal autonomic cephalalgia 4. Other primary headache disorders 4.1 Primary cough headache 4.2 Primary exercise headache 4.3 Primary headache associated with sexual activity 4.4 Primary thunderclap headache 4.5 Cold-stimulus headache 4.6 External pressure headache 4.7 Primary stabbing headache 4.8 Nummular headache 4.9 Hypnic headache 4.10 New daily persistent headache (NDPH) 5. Headache attributed to trauma or injury to the head and/or neck 5.1 Acute headache attributed to traumatic injury to the head 5.2 Persistent headache attributed to traumatic injury to the head 5.3 Acute headache attributed to whiplash 5.4 Persistent headache attributed to whiplash 5.5 Acute headache attributed to craniotomy 5.6 Persistent headache attributed to craniotomy

Contd ... 6.2 Headache attributed to non-traumatic intracranial hemorrhage 6.3 Headache attributed to unruptured vascular malformation 6.4 Headache attributed to arteritis 6.5 Headache attributed to cervical carotid or vertebral artery disorder 6.6 Headache attributed to cerebral venous thrombosis (CVT) 6.7 Headache attributed to other acute intracranial arterial disorder 6.8 Headache attributed to genetic vasculopathy 6.9 Headache attributed to pituitary apoplexy 7. Headache attributed to non-vascular intracranial disorder 7.1 Headache attributed to increased cerebrospinal fluid pressure 7.2 Headache attributed to low cerebrospinal fluid pressure 7.3 Headache attributed to non-infectious inflammatory disease 7.4 Headache attributed to intracranial neoplasia 7.5 Headache attributed to intrathecal injection 7.6 Headache attributed to epileptic seizure 7.7 Headache attributed to Chiari malformation type I (CM type I) 7.8 Headache attributed to other non-vascular intracranial disorder 8. Headache attributed to a substance or its withdrawal 8.1 Headache attributed to use of or exposure to a substance 8.2 Medication-overuse headache (MOH) 8.3 Headache attributed to substance withdrawal 9. Headache attributed to infection 9 .1 Headache attributed to intracranial infection 9.2 Headache attributed to systemic infection

6.1 Headache attributed to ischemic stroke or transient ischemic attack

10. Headache attributed to disorder of homoeostasis 10.1 Headache attributed to hypoxia and/ or hypercapnia 10.2 Dialysis headache 10.3 Headache attributed to arterial hypertension 10.4 Headache attributed to hypothyroidism 10.5 Headache attributed to fasting 10.6 Cardiac cephalalgia 10.7 Headache attributed to other disorder of homoeostasis

Contd ...

Contd ...

6. Headache attributed to cranial or cervical vascular disorder

25

Evaluation of Headache

Table 4.2: The headache classification (modified) (numbers refer to the ICHD-3 code)4·6·7 Contd...

11. Headache or facial pam attnbuted to disorder of the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical structure 11.1 Headache attributed to disorder of cranial bone 11.2 Headache attributed to disorder of the neck 11.3 Headache attributed to disorder of the eyes 11.4 Headache attributed to disorder of the ears 11.5 Headache attributed to disorder of the nose or paranasal sinuses 11.6 Headache attributed to disorder of the teeth or jaw 11.7 Headache attributed to temporomandibular disorder (TMD) 11.8 Head or facial pain attributed to inflammation of the stylohyoid ligament 11.9 Headache or facial pain attributed to other disorder of cranium, neck, eyes, ears, nose, sinuses, teeth, mouth or other facial or cervical structure 12. Headache attributed to psychiatric disorder 12.1 Headache attributed to somatization disorder 12.2 Headache attributed to psychotic disorder 13. Painful cranial neuropathies and other facial pains 13.1 Trigeminal neuralgia 13.2 Glossopharyngeal neuralgia 13.3 Nervus intermedius (facial nerve) neuralgia 13.4 Occipital neuralgia 13.5 Optic neuritis 13.6 Headache attributed to ischemic ocular motor nerve palsy 13.7 Tolosa-Hunt syndrome 13.8 Paratrigeminal oculosympathetic (Raeder's) syndrome 13.9 Recurrent painful ophthalmoplegic neuropathy 13.10 Burning mouth syndrome (BMS) 13.11 Persistent idiopathic facial pain (PIFP) 13.12 Central neuropathic pain 14. Other headache disorders 14.1 Headache not elsewhere classified 14.2 Headache unspecified

Table 4.3: Common causes of headache1·8

Primary headache Tension-type 69% Migraine 16% Idiopathic Stabbing 2% Exertional 1 % Cluster 0.1 %

Secondary headache Systemic infection 63% Head injury 4% Vascular disorders 1 % Subarachnoid hemorrhage

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Clinical Methods in Pain Medicine

48

Algorithm2 Neck pain with headache/cervicogenic headache

Limited neck movements, dull aching pain, trigger points present, tenderness over muscles

Sharp shooting pain and tenderness along the distribution of GON, LON or 3rd occipital nerve

Pain well localized, increases on neck extension, lateral flexion and rotation

Predominant headache, fixed duration of attack, associated prodromal and aura symptoms

MFS

Occipital neuralgia

FJA

Migraine

MFS-myofascial pain syndrome; FJA-facet joint arthropathy; GON-greater occipital nerve; LON-lesser occipital nerve.

c. Abdominal: Palpation of abdominal organs for enlargement and infection. INVESTIGATIONS

1. Routine blood investigation with ESR

and CRP: It should be done in all cases suspecting inflammatory arthropathy. 2. X-ray, AP and lateral view: Bony changes are well recognized by X-rays, hence can identify fractures, degenerative osteophytes and cervical rib. 3. CT scan: Bony abnormalities, hemorrhage can be seen well with CT scan and advised in trauma cases, facet joint and uncovertebral joint abnormalities. 4. MRI: Soft tissue like disc, nerve root, canal diameter, muscles, vascular aneurysm and abnormalities are best seen on MRI. 5. Diagnostic blocks: It helps in finding pain generators. Various blocks can be performed and are evidence based. More than 50% pain relief is considered positive. a. Occipital nerve block-in case of occipital neuralgia, but can be positive in migraine and tension type headache. b. Medial branch block-for facet joint arthropathy.

c. Cervical interlaminar epidural injections-in case of radiculopathy and prolapsed disc. d. Trigger point injections in myofascial pain syndrome. e. Stellate ganglion block in case of CRPS. 6. EMG and NCV: These studies will be abnormal when nerves are involved, especially larger fibers and abnormal in radiculopathy and nerve entrapment syndromes. In CRPS, these studies are usually normal. 7. Ultrasound neck and shoulder done when muscles and tendon tear are suspected.

I REFERENCES 1. Fishman SM, Ballantyne JC, Rathmell JP. Bonica's Management of Pain; 4th edn. Philadelphia, Lippincott Williams & Wilkins, Wolters Kluwer, 2010; p. 1020-8. 2. Fauci AS, Braunwald E, Kasper DL, et al (Eds). Harrison's Principles of Internal Medicine; 18th edn. New York, McGraw-Hill, 2012; p. 140. 3. Gary S, Firestein GS, Ralph C, et al. Kelley's Textbook of Rheumatology; 9th edn. Philadelphia, Elsevier, 2013; p. 628-37. 4. Kelley WN, Harris ED (Jr), Ruddy S, et al (Eds). Textbook of Rheumatology; 5th edn. Philadelphia, WB Saunders, 1997; p. 394.

Evaluation of Neck Pain

5. Crockard HA. Surgical management of cervical rheumatoid problems. Spine 1995;20: 2584-90. 6. Frobert 0, Fossgreen J, et al. Musculoskeletal pathology in patients with angina pectoris and normal coronary angiograms. J Intern Med 1999;245:237-46. 7. Hans van Suijlekom, Nagy Mekhail, Nileshkumar Patel, et al. Pain practice 2010;10(2):131-6. 8. Sforza C, Grassi G, et al. Three-dimensional analysis of active head and cervical spine

49

range of motion: Effect of age in healthy male subjects; Clin Biomech (Bristol, Avon) 2002; 17:611-4. 9. Weinfeld RM, Olson PN, et al. The prevalence of diffuse idiopathic skeletal hyperostosis (DISH) in two large American Midwest metropolitan hospital populations. Skeletal Radial 1997;26:222-5. 10. Steven D. Waldman. Pain Management; 2nd edn. Philadelphia, Elsevier, Saunders, 2011; p. 526.

Chapter

6 Evaluation of Shoulder Pain Tarun Kumar Reddy, Rammurthy Kulkarni

INTRODUCTION

2. Cervical spinal canal stenosis 3. Long thoracic and suprascapular neuralgia 4. Postherpetic neuralgia involving C4, 5 nerve roots 5. CRPS involving upper arm and shoulder. 6. Referred pain i. Myofascial pain syndrome (commonly trapezius) 11. Diaphragm irritation iii. Myocardial ischemia iv. Intrathoracic tumors

Shoulder pain is the third-leading cause for patients seeking musculoskeletal care.1,2 The impact of shoulder pain on health-related quality of life is also substantial. It is important to obtain the history, physical examination and relevant investigation, which are essential in making the diagnosis. For many disease entities, a diagnosis can be accurately reached even without the use of imaging studies.3 In this chapter an overview of common causes of shoulder pain and basic clinical approach to diagnosis them have been discussed.

Traumatic

• • • •

CLASSIFICATION

The causes for shoulder pain can be classified as follows.

Fracture clavicle Fracture humerus Glenohumeral dislocation Acromioclavicular ligament sprain

Non-traumatic HISTORY

Intrinsic Causes

The first step in diagnosing the cause of shoulder pain is taking a thorough history. Readers can refer to Chapter 2 for basic concepts on history taking. Initially, all the red flag indicators should be ruled out.

1. Glenohumeral

i. Rotator cuff tendinopathy. 1i. Rotator cuff tear iii. Subacromian bursitis iv. Glenohumeral arthritis v. Glenohumeral instability vi. Labral rear 2. Extra glenohumeral i. Bicipital tendinopathy ii. Acromioclavicular arthritis iii. Subscapular bursitis iv. Distal clavicle osteolysis.

Red Flags These include

• • • • •

Tumor Acute rotator cuff tear Unreduced dislocation Infection Unexplained significant sensory and motor deficit • Pulmonary or vascular compromise.

Extrinsic Causes 1. Disc herniation with neural impinge-

ment at C5 or C6 level 50

Evaluation of Shoulder Pain

The following issues should be covered in history Age: Instability is more common with age less than 35 years whereas rotator cuff and glenohumeral pathologies are common an age more than 35 years. Trauma: Any significant trauma or any strenuous activity that preceded the pain should be asked. Fracture and traumatic rotator cuff tear may have pain immediately, but adhesive capsulitis tends to have a more gradual onset. Pain history: History should be targeted at onset, nature, duration, exacerbating and relieving factors, quality, location, and radiation which helps in diagnosis. Some important facts on shoulder pain are discussed below. • Location of pain should be noted. Anterolateral shoulder pain is often associated with impingement syndrome and the various stages of rotator cuff tendinopathy. However, rotator cuff tendinopathy involving the external rotators (teres minor and infraspinatus) can cause focal pain on the posterior shoulder, or sometimes referred pain over the scapula. Pain that is poorly localized is often extrinsic (referred pain). • Activities that exacerbate symptoms either at work (lifting overhead, painting) or leisure activity (racquet sports, swimming) can indicate rotator cuff pathologies and impingement syndrome. • Nocturnal pain and difficulty sleeping on affected side. Bony pain or malignancy should be considered in these patients. However, patients with rotator cuff tear can also have night pain. • Ask for any neck pain, thoracic pain, or other radiating pain in the upper limb. Any history of (H/ o) tingling and numbness along the upper limb. Radicular pain with motion crossing the elbow to the hand and wrist may indicate lower cervical involvement. However, CS root involvement may manifest as isolated shoulder pain. It is essential to have a high index of suspicion for cervical

51

spine disease as a cause of the painful shoulder. • Ask for impact on the function of the joint. What activities are impaired? History of limited reaching (e.g. reaching for a jar on the top shelf, across the chest) and limited rotation (e.g. unable to scratch the back, difficulty putting on a coat). Pain in bringing hand across the chest may be seen in acromioclavicular pathology. • Ask for other joint involvement. Any trigger points. Any tender areas. Past history: History of shoulder pain or any other musculoskeletal disorders and their response to treatment should be noted. History of stiffness or restricted motion suggests adhesive capsulitis, and glenohumeral arthritis. History of previous surgeries in the shoulder or previous injections in the shoulder should be noted down. Significant comorbid history: Disease like diabetes, stroke, cancer, respiratory, gastrointestinal, renal disease and ischemic heart disease should be ruled out for possible cause and also the chance of referred pain. Systemic illness: Fever, night sweats, weight loss, rash and respiratory symptoms should be enquired Treatment history: History of current drug treatment and any adverse reactions should be noted down. PHYSICAL EXAMINATION

A complete physical examination includes inspection, palpation, assessment of range of motion, strength and special tests. 4 The neck and the elbow also should be examined to exclude the possibility of referred pain in shoulder region from a pathologic condition in either of these regions. Inspection

Inspect shoulders from front, side and back for muscle wasting and atrophy, abnormal swelling, deformity (dislocations), scars, ecchymosis and venous distension. Always compare with the opposite normal shoulder.

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Clinical Methods in Pain Medicine

Atrophy of the supraspinatus or infraspinatus should prompt a further work-up for such conditions as rotator cuff tear, suprascapular nerve entrapment or neuropathy. Deformity, such as squaring off the shoulder that occurs with anterior dislocation, can immediately suggest a diagnosis. Scapular "winging", which can be associated with shoulder instability and serratus anterior or trapezius dysfunction, should be noted. Look at neck and axillae for lymphadenopathy. Palpation

Palpation includes glenohumeral joint, acromioclavicular and sternoclavicular joints, cervical spine, rotator cuff and bicipital groove. The coracoid process, acromion and scapula should also be palpated for any tenderness and deformity. Specific localized tenderness will aid us in diagnosis. Compare with opposite normal shoulder. If fibromyalgia is suspected then palpate for any tender points. Range of Motion

Range of motion should be assessed for forward flexion, isolated abduction, horizontal adduction, external rotation and internal rotation with arm at 0°, and external rotation

and internal rotation with the arm in abduction. Range of motion on the affected side should be compared with that on the normal side. Apley' s scratch test can be used to test the range of motion (Figs 6.1 and 6.2). Passive horizontal adduction and abduction can exacerbate pain in acromioclavicular joint pathology. One can get an idea of whether the problem is in the rotator cuff or the glenohumeral joint by testing the patient's range of motion. If the patient cannot move his or her arm through, its full active range of motion, then the examiner should assess for a difference between passive motion and active motion. Glenohumeral problems will limit both active motion and passive motion in forward elevation, internal rotation, and external rotation. Impingement syndrome and rotator cuff tears will limit the patient's active motion, but the passive motion should not be much different than in the normal shoulder. A painful arc between 70° to 120° abduction is seen in subacromian pathology. Pain can often inhibit full passive motion, so it is recommended to keep patient supine while tests forward elevation or external rotation and these motions are abnormal in sitting position. In supine position, the patient

Figs 6.1 and 6.2 Apley scratch test. The patient attempts to touch the opposite scapula to test range of motion of the shoulder

(left). Testing abduction and external rotation (right). Testing adduction and internal rotation

53

Evaluation of Shoulder Pain

is less likely to contract his or her shoulder muscles while the examiner moves the arm, thereby causing less pain. Muscle Strength

A key finding, particularly with rotator cuff problems, is pain accompanied by weakness. True weakness (e.g. rotator cuff tear) should be distinguished from weakness due to pain. The lidocaine injection test in the subacromial bursa is indicated to distinguish true weakness from weakness due to pain. Patients with a rotator cuff tear will have persistent weakness despite pain relief with injection, while those with rotator cuff tendinopathy will have normal strength in association with pain relief. The following tests are done to check the rotator cuff muscle strength. Empty Can Test5,

• • • •

alternative to the lift-off test7 for shoulders that had decreased internal rotation. Posture: Patient in sitting posture with hand of the affected arm placed on the abdomen. Fixation: No fixation is applied. Test: Patient exerts pressure on the abdomen with the hand until maximal internal rotation (Fig. 6.4). Pay attention: The patient feels weakness and cannot maintain maximal internal rotation. The elbow drops backwards, and internal rotation is lost. Pressure is exerted by extension of shoulder and flexion of the wrist.

31

• Background: To test the strength of supraspinatus muscle. The subscapularis, infraspinatus and teres minor are electrically comparatively silent on this position. • Posture: Sitting or standing, shoulders in 90° abduction, 30° of horizontal adduction and full internal rotation. • Fixation: The examiner places his hands on the upper side of the limb and exerts downward resistance. • Test: The patient maintains this position against downwards resistance (Fig. 6.3). • Pay attention: Focus primarily for muscle weakness and less attention to pain. Belly Press Test': 31

• Background: The belly press test may be valuable as specific test to rule out subscapular tears. The test was designed as an

Fig. 6.3 Empty can test

Fig. 6.4 Belly press test

To test infraspinatus and teres minor strength31 • Background: To test infraspinatus and teres minor strength. • Posture: Patient arms by the side with elbows flexed at 90°. • Fixation: Examiner keeps his hands on the side of the arm. • Test: Patient is asked to externally rotate the arm against the examiners hand resistance (Fig. 6.5). • Pay attention: The patient's external rotation strength is compared to normal arm.

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Clinical Methods in Pain Medicine

Fig. 6.5 Test to check the strength of infraspinatus and teres minor

Hawkins-Kennedy Test13,

Special Tests

1. Impingement tests: Impingement is one of the most frequently described pathological shoulder conditions in general practice and in sports medicine.8 Early literature described impingement as a pathology or a diagnosis9 but today impingement is considered to be a cluster of symptoms, rather than pathology itself. Rotator cuff pathology.!? scapular dyskinesis, shoulder instability,11 biceps pathology have been suggested to cause shoulder impingement symptoms. Neer's Test12•

Fig. 6.6 Neer's test

13

• Background: The greater tubercle impinges the degenerated supraspinatus and subacromial bursa against the acromion. • Posture: Patient in either sitting or standing posture and examiner is standing. • Fixation: Fix ipsilateral scapula to prevent protraction. • Test: Passive forward elevation of the arm (Fig. 6.6). • Pay attention: Focus on pain in the shoulder. The pain is relieved by injecting 10 ml of lidocaine beneath the anterior acromion.

14

• Background: The greater tuberosity forces the supraspinatus tendon against the coracoacromial ligament. • Posture: Patient in seated or standing posture, with arm in 90° in forward elevation in the scapular plane. • Fixation: Stabilise the scapula to minimise upward rotation during performance of the internal rotation maneuver. • Test: Passive internal rotation of the shoulder is done until pain occurs (Fig. 6.7). • Pay attention: Focus for pain with forced internal rotation.

Fig. 6.7 Hawkin's test

55

Evaluation of Shoulder Pain

2. Rotator cuff tests: The following tests are done to identify the rotator cuff tears. The external rotation lag sign is having more specificity for supraspinatus and infraspinatus tears. The drop arm test produces a few false positives. Drop Arm Test13•

15

• Background: Originally this test was designed for the assessment of supraspinatus tendon tears. Later on, the test was also used to assess infraspinatus tears. • Posture: Patient is lying supine or sitting with the arm next to the body. • Fixation: No fixation is applied. • Test: The patient abducts the arm horizontally in the plane of scapula. Then ask the patient to lower the arm (Figs 6.8 and 6.9). • Pay attention: During the descent to the anatomical position the patient may lean to the affected side and may lower the whole arm quite suddenly.

External Rotation Lag Sign13,

16

• Background: A lag sign is suggestive of a (partial) tear of the infraspinatus or supraspinatus tendons. • Posture: Patient is seated with the back towards the examiner. The shoulder is moved to 20° abduction, the elbow 90° flexion and maximal external rotation. • Fixation: The examiner supports the elbow and holds the wrist. • Test: The patient is asked to maintain this position, while the examiner releases the wrist (Figs 6.10 and 6.11). • Pay attention: Focus on the capacity of the patient to hold the arm in the same position. When an angular drop (lag sign) occurs, the test is positive. 3. Tests to diagnose shoulder instability: The apprehension, relocation and anterior release tests all appear to be diagnostic of anterior instability, especially when 'apprehension' is used as a positive test.

Figs 6.8 and 6.9 Drop arm test

Figs 6.10 and 6.11 External rotation lag sign

Clinical Methods in Pain Medicine

56

Apprehension Test13•

17

• Background: The combined motion and









anterior directed pressure causes subluxation of the shoulder. Posture: Patient is kept in a supine or sitting position with shoulder in 90° abduction and maximal external rotation. Fixation: The examiner holds the wrist of the patient with one hand. The other hand is placed on the posterior aspect of the humeral head. Test: Maximal external rotation is applied and the posterior aspect of the humeral head is also pressed forward (Fig. 6.12). Pay attention: Focus on sudden apprehension feeling in the shoulder and pain.

Fig. 6.13 Relocation test

Anterior Release Test13,

19

• Background: On releasing the posteriorly

directed force, the humeral head can subluxate anteriorly. • Posture: The patient is kept in supine

position with arm in 90° abduction and the elbow in 90° flexion. • Fixation: The examiner holds the forearm

with one hand and other hand is placed on the anterior part of humeral head. • Test: The examiner places a posteriorly

Fig. 6.12 Apprehension test

Relocation Test13• 18 • Background: The posterior directed force

maintains the humeral head in position.

directed force to the humeral head, while the arm is brought to extreme external rotation. The humeral head is then released (Fig. 6.14). • Pay attention: Focus for sudden pain,

an increase in pain or an apprehension feeling.

• Posture: The patient is kept in a supine

position with arm in 90° abduction and the elbow in 90° flexion. • Fixation: The examiner holds the forearm

with one hand and the other hand is placed on the humeral head. • Test: The examiner externally rotates the shoulder levering the forearm with one hand. The other hand applies a posterior force to the humeral head (Fig. 6.13). • Pay attention: Focus on pain relief and ability to tolerate maximal external rotation.

Fig. 6.14 Anterior release test

57

Evaluation of Shoulder Pain

4. Tests to diagnose acromioclavicular (AC)

pathology: For acromioclavicular joint pathology, the O'Brien test can be used as a confirmatory test due to the test's high specificity. Palpation of the AC joint can be used to rule out AC complaints when the test is negative, since the sensitivity of this test is high. O'Brien Test13,

20

• Background: The acromion is pushed by the tuberculum majus, compressing the AC joint. • Posture: Patient in standing posture with arm in 90° forward flexion, 10-15° adduction and full internal rotation and the examiner stands behind the patient. • Fixation: The examiner puts their hand on the forearm of the patient. • Test: Examiner applies downward force to the lower arm and the patient resists this

force. After this, the palm of the patient's hand is supinated, and the test is repeated (Figs 6.15 and 6.16). • Pay attention: Focus for pain around the acromioclavicular (AC) joint, which is more with resisted internal rotation. AC Joint Tenderness Test13, 21

• Procedure: The test is positive if a recognizable pain is felt on palpation. It has a sensitive value of 96% and specificity of 10%.

5. Tests to diagnose bicipital tendinitis: On physical examination, the most common finding is point tenderness in the bicipital groove. The point of tenderness should move as the shoulder is passively internally and externally rotated. Other provocative tests that are specific for bicipital tendinitis include the Speed test and the Yergason test. Speed Test13

• Posture: Patient in standing position and the examiner stands in front of the patient. The shoulder is positioned in 90° of forward Hexion with the elbow extended, and forearm supinated. • Fixation: The examiner puts his hand on the forearm of the patient. • Test: The examiner applies downward force to the arm and the patient resists this force (by trying to flex) (Fig. 6.17).

Figs 6.15 and 6.16 O'Brien test

Fig. 6.17 Speed test

Clinical Methods in Pain Medicine

58

• Pay attention: Focus for pain in the bicipital groove. • Background: When this test is positive, bicipital tendinitis can be suspected. Yergason Test13

When performing the Yergason test, the patient supinates the forearm against resistance with the forearm flexed (Fig. 6.18). The test is a positive test result when pain refers to the bicipital groove.

films are obtained in a patient with a history of trauma, both AP and axillary views are warranted since some conditions can be missed on the former alone. Plain films can identify the following: • Fractures of the proximal humerus, clavicle, and scapula • Glenohumeral dislocations • Glenohumeral osteoarthritis • AC joint arthritis or injury • Sternoclavicular (SC) joint arthritis Magnetic Resonance Imaging (MRI)

Fig. 6.18 Yergason test

MRI is the preferred imaging study in patients with suspected impingement and rotator cuff injury. A normal MRI suggests that the likelihood of a rotator cuff tear is less than 10%.22, 23 On the other hand, MRI findings for rotator cuff tears are not highly specific, particularly in older patients.24 The sensitivity and specificity of MRI for the diagnosis of impingement are approximately 93 and 87%, respectively.25 MRI is also useful in the evaluation of avascular necrosis, biceps tendinopathy and rupture, inflammatory processes and tumors.26

INVESTIGATIONS

Diagnostic imaging of the shoulder may be valuable when directed by the history and physical examination. A variety of modalities may be employed. Complete blood count, rheumatological profile may be ordered if needed.

Ultrasonography

At the hands of skilled operators, the diagnostic accuracy of ultrasound has been found to be the equivalent of MRI in identifying rotator cuff tears, labral tears, and biceps tendon tears and dislocations.P=P' Ultrasound is less expensive than MRI and preferred by patients.F" 30

Plain Radiograph

Plain radiographs of the shoulder generally have limited benefit in the evaluation of nontraumatic shoulder pain. While there are no specific guidelines for when radiography is indicated, it is generally recommended to obtain plain films in patients who have lost range of motion, particularly when there is severe pain, and after trauma. When plain

Interventions (Diagnostic Blocks)

Stellate ganglion block and T2/T3 sympathetic block can be used as diagnostic injections when shoulder hand syndrome is suspected. If radiculopathy is suspected, then a selective nerve root block can be done. If myofascial pain syndrome is suspected then trigger point injections can be given.

59

Evaluation of Shoulder Pain

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" 95% of patients, usually at the onset of symptoms. A few patients develop ANA within 1 year of symptom onset; repeated testing may thus be useful. ANA-negative lupus exists but is very rare in adults, and is usually associated with other autoantibodies (anti-Roor anti-DNA). Hightiter IgG antibodies to double-stranded DNA (dsDNA) (but not to singlestranded DNA) are specific for SLE. 4. Other markers a. HLA B27: It is mostly positive in anky-

losing spondylitis and other spondyloarthropathies. The presence of HLA B27 is neither necessary nor sufficient for the diagnosis. However, in accord with

178

Clinical Methods in Pain Medicine

Bayes' theorem, the presence or absence of HLA B27 greatly increases or decreases, respectively, the probability of ankylosing spondylitis in patients with equivocal clinical findings lacking radiographic abnormalities. b. Thyroid markers: Thyroid stimulating hormone (TSH), T3, T4 should be ordered if hypothyroidism is suspected. c. Creatine kinase (CK): Levels should be checked if polymyositis (PM) or dermatomyositis (DM) is suspected. The most sensitive enzyme is CK, which in active disease can be elevated by as much as 50-fold. Although the CK level usually parallel disease activity, it can be normal in some patients with active DM, especially when associated with a connective tissue disease. The CK is always elevated in patients with active PM. 5. Synovial fluid analysis: Synovial fluid analysis confirms the presence of inflammatory arthritis, although none of the findings are specific. The fluid is usually turbid, with reduced viscosity, increased protein content, and a slightly decreased or normal glucose concentration. The white cell count varies between 5 and

50,000 I µl; PMNLs predominate. A synovial fluid white blood cell count> 2000 / µl with > 75% polymorphonuclear leukocytes is highly characteristic of inflammatory arthritis, although not diagnostic of RA. Total hemolytic complement, C3 and C4 are markedly diminished in synovial fluid relative to total protein concentration as a result of activation of the classic complement pathway by locally produced immune complexes. 6. Radiographic evaluation: X-ray is useful in rheumatoid arthritis. Early in the disease, radiographic evaluations of the affected joints are usually not helpful in establishing a diagnosis. As the disease progresses, abnormalities become more pronounced, but none of the radiographic findings is diagnostic of RA. The diagnosis, however, is supported by a characteristic pattern of abnormalities, including the tendency toward symmetric involvement. Juxta-articular osteopenia may become apparent within weeks of onset. Loss of articular cartilage and bone erosions develops after months of sustained activity. The primary value of radiography is to

ALGORITHMS Algorithm 1 Chronic widespread pain Rule out red flags

Pain after exertion morning stiffness +/joint swelling-ESR and CRP normal possible systemic symptoms

Non-inflammatory

Urgent referral

Pain worse after rest night pain+ morning stiffness >30 minutes joint swelling + increased ESR and CRP possible systemic symptoms

Inflammatory

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Evaluation of W idespread Pain

determine the extent of cartilage destruction and bone erosion produced by the disease, particularly when one is attempting to

estimate the aggressive nature of the disease, monitoring the impact of therapy with disease modifying drugs.

Algorithm 2 Non-inflammatory

H/o excessive fatigue H/o unrefreshed sleep H/o memory impairment Multiple somatic symptoms (text)

H/o depressive features H/o somatoform disorder

DSM-IV criteria and psychiatry referral Use ACR 2010 criteria (see text)

Diagnose fibromyalgia

• Patient counseling • Regular exercise • Anticonvulsants • SNRls

Both fibromyalgia and depression

• Treat fibromyalgia • Psychiatry referral

Diagnose major depression +/somatoform disorder

• Patient counseling •SSRls • Psychiatry referral

Algorithm 3 Inflammatory

Mainly small joint involved symmetrical, RA factor +/-, anti-CCP +, erosions in X-ray and other systemic symptoms

Skin rash (face), muscle pain, joint pain (arthritis), fatigue and other systemic features

Use ACR 2010 criteria

ANA+

Creatine kinase +

Diagnose rheumatoid arthritis

Suspect SLE

Suspect polymyositis or dermatomyositis

Refer to rheumatologist

Refer to rheumatologist

Disease modifying drugs, analgesics and alternate day steroid +/No improvementrheumatologist

Muscle pain, muscle weakness (proximal), muscle atrophy +/and skin rash

Clinical Methods in Pain Medicine

180

Algorithm 4 Inflammatory

History of: • Weight gain • Hoarseness of voice • Cold intolerance • Puffy face, dry skin • Irregular menstrual cycles

Increased TSH decreased free T3, T4

Axial spine involved Alternating buttock pain Early morning pain Night pain Peripheral large joints +/-

Chest expansion decreased HLA B27 + X-ray/MRl-sacroiliitis

Suspect hypothyroidism Spondyloarthropathies (ankylosing spondylitis) Refer to rheumatologist Exercises/yoga DMDs +/analgesics

I REFERENCES 1. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia. Report of the multicenter criteria committee. Arthritis Rheum 1990;33(2):160-72. 2. Mease P, Arnold LM, Choy EH, et al. Fibromyalgia syndrome. J Rheumatol 2007 Jun; 34( 6): 1415-25. 3. Bergman S. Psychosocial aspects of chronic widespread pain and fibromyalgia. Disabil Rehabil 2005;27(12):675-83. 4. White KP, Speechley M, Harth M, et al. Comparing self-reported function and work disability in 100 community cases of fibromyalgia syndrome versus controls in London, Ontario: The London fibromyalgia epidemiology study. Arthritis Rheum 1999; 42(1):76-83. 5. Henriksson CM, Liedberg GM, Gerdle B. Women with fibromyalgia: Work and Rehabilitation. Disabil Rehabil 2005;27(12):685-94. 6. Clauw DJ. Fibromyalgia: Update on mechanisms and management. J Clin Rheumatol. 2007;13(2):102-9. 7. CroftP,SchollumJ, Silman A. Population study of tender point counts and pain as evidence of fibromyalgia BMJ 1994;309(6956):696-9.

8. Jacobs JW, Rasker JJ, van der Heide A, et al. Lack of correlation between the mean tender point score and self-reported pain in fibromyalgia. Arthritis Care Res 1996;9(2):105-11. 9. Okifuji A, et al. A standardized manual tender point survey. Development and determination of a threshold point for the identification of positive tender points in fibromyalgia syndrome. Journal of Rheumatology 1997;24(2): 377-83. 10. Bidari AB, Ghavidel-Parsa, Ghalehbaghi B. Reliability of ACR criteria over time to differentiate classic fibromyalgia from nonspecific widespread pain syndrome: A 6-month prospective cohort study. Mod Rheumatol 2009; 19(6):663-9. 11. Wiesinger T, Smolen JS, Aletaha D, et al. Compression test (Gaenslen's squeeze test) positivity, joint tenderness and disease activity in patients with rheumatoid arthritis. Arthritis Care Res (Hoboken) 2013 Apr; 65(4): 653-7. 12. Nishimura K, Sugiyama D, Kogata Y, et al. Meta-analysis: Diagnostic accuracy of anticyclic citrullinated peptide antibody and rheumatoid factor for rheumatoid arthritis. Ann Intern Med 2007 Jun 5;146(11):797-808.

Chapter

16 Psychological Evaluation Ayanangshu Nayak

Patients suffering from chronic pain frequently experience psychological or emotional difficulties. Such difficulties commonly include depressive episodes, various anxiety disorders, adjustment disorders or other stress related conditions. Statistically, these conditions are significantly more prevalent compared to their prevalence in the general population.l 2 For instance various population surveys predict doubling of depression rate in people suffering from chronic pain.3 Moreover, research suggests that depression is closely associated with poor life satisfaction in patients suffering from chronic pain.v'' Hence, it is vital that psychological issues are identified and treated as early as possible in work up of chronic pain. However, these are not the only conditions seen in patients presenting in a chronic pain service. Expected levels of correlation, predicted from the population surveys of various functional psychiatric conditions such as schizophrenia or bipolar disorder are seen. Some recent studies however show a more than expected correlation between chronic pain and bipolar disorder.6 If warranted or if suspected, a psychiatric referral should be initiated for these patients. Other psychological conditions such as patients with dissociative or somatoform pain disorder or fabrication illnesses may sometimes present in the pain clinic. Usually, a diagnosis or possibility of either condition should result in a referral for psychiatric assessment. 181

A further set of psychological difficulties are relatively common in patients suffering from chronic pain. First of these is psychosexual and relationship difficulties which according to some evidence are twice as common if a partner suffers from a chronic pain condition compared to the general population prevalence.7 Some of these conditions are due to the illness resulting in chronic pain. For instance, spinal cord injuries sometimes result in chronic pain as well as psychosexual difficulties. Not only the patients but their partners are also affected. Due to embarrassment many patients find it difficult to talk about the issue and hence proactive yet sensitive questions from the assessors may elicit the full set of difficulties. Sometimes, patients' partners may also need referral for individual or couples' work arising from such assessments. Psychosexual difficulties may also be iatrogenic. For instance, opiates at times cause hyperprolactinemia resulting in lower testosterone levels. Both can reduce sexual drive. The demographic profile of patients reporting chronic pain and sexual and relationship difficulties hints however at a more complex inter-relationship. For instance, many studies report a higher incidence of childhood sexual abuse history in patients presenting to a chronic pain service.8 Finally, substance misuse is a common issue among chronic pain clinic patient cohorts. Ranging from abuse or harmful use to full dependence syndrome, the substances used are not only prescribed or illicit opiates or

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benzodiazepines but other substances of abuse such as alcohol or stimulants (cocaine, speed or cannabinoids). Some substance misuse clinicians prefer to classify these patients depending on the long-term history of abuse (independent of the chronic pain condition) as well as by reward seeking behavior rather than inappropriate use of analgesics for more effective pain relief. However, both sets of patients suffer from dependence syndrome which is virtually identical in presentation in the clinical practice, if not in prognosis. It is difficult to tease out if this hypothesis is true or not due to obvious methodological difficulties in devising a suitable study. However, in any assessment reason for ongoing substance use must be enquired.9 These patients difficulties are usually challenging for everyone concerned and these patients need multidisciplinary team input. In addition to the conditions listed above a further set of patients present with other psychosocial difficulties. Upset or anger with a victim mind-set can be present with or without comorbid depression or anxiety related difficulties. The distress can increase if litigation is involved.l'' Unpleasantness in mood (dysphoria) related to these are commonly mistaken for depression. Careful history or non-response to usual treatment for depression should alert clinicians to rule out these issues. Identifying such social issues are important as prognosis depends on their presence or absence. Once identified, talking treatments or psychotherapy can sometimes help these patients move forward in their ability to function as meaningful members of the family or the society in general. However, one has bear in mind that stressful life events are risk factors for clinical depression. Assessment: Screening at the Clinical Interview

Pain clinicians should routinely screen for common psychiatric disorders such as depression or anxiety. Many standard clinical questions have been evaluated in research settings for anxiety or depression. National

Institute for Health and Clinical Excellence (NICE) in 2009 recommended using the following two questions to screen for depression: 1. During the last month have you been feeling down, depressed or hopeless? 2. During the last month have you often been bothered by having little interest or pleasure in doing things? In various studies in different settings the sensitivity and specificity of these two questions has been found to be over 95% and between 75 and 85% respectively.11 Of course further onward psychiatric referral must then be ensured for patients answering yes to both the questions above. Similarly, there is a two-question screening for core anxiety symptoms. Kroenke, et al.12 found high sensitivity for generalized anxiety disorder or panic disorder to the following: How often have you been bothered by 1. Being nervous, anxious or on edge? 2. Not being able to stop or control worrying? Clinical questions often help elicit or rule out dependence syndrome and all initial assessments should aim to check for tolerance and withdrawal features. Blood or urine tests are useful when suspicion is raised about opiate or alcohol dependence. FORMAL SCREENING TOOLS

There are specific screening tools for use in this patient population. An earlier chapter describes some of these. Self-rated tools are more useful for non-psychiatry clinicians. For instance, Beck's Depression Inventory or Primary Health Questionnaire-9 (9 item scale, PHQ-9) and PHQ-15 are useful for detecting depression. GAD-7 has sufficient sensitivity and specificity for detecting anxiety or panic disorder, whereas GAD-2 can be useful in screening for generalized anxiety disorder, panic disorder, phobias as well as posttraumatic stress disorder (EBM-BMJ 2007; 12). Similarly, Addiction Severity Index (ASI) and

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Anger Expression Inventory (AEI) have been used in research in chronic pain. There are some screening tools which are specifically validated and devised for use in physical health care settings. Hospital Anxiety and Depression Scale (HADS) devised by Snaith and Zigmond, for instance, can screen for both conditions and the questions generally avoid biological symptoms associated with these conditions. One has to keep in mind that these, however, are just screening tools and are not replacements for formal face to face

psychiatric interviews and can at best inform clinicians to focus or prioritize treatment need of the individual patients. However, these tools can be used to document or check for the effectiveness of the treatment. In addition to these psychological screening tools disability component in a pain inventory (such as brief pain inventory) are used by the mental health professionals to check for the effectiveness of the treatment offered. GAD-7, PHQ-9 and PHQ-15

GAD-7 Over the last 2 weeks, how often have you been bothered by the following problems? (Use"../" to indicate your answer). 1. Feeling nervous, anxious or on edge

2. 3. 4. 5. 6. 7.

Not being able to stop or control worrying Worrying too much about different things Trouble relaxing Being so restless that it is hard to sit still Becoming easily annoyed or irritable Feeling afraid of as if something awful might happen

Not at all

Several days

1 0 1 0 1 0 0 1 0 1 0 1 1 0 (For office coding: Total Score T

More than half the days

Nearly everyday

2 3 2 3 2 3 2 3 2 3 2 3 2 3 ....... = ....... + ....... + ....... )

Scores of 5, 10, and 15 represent cut points for mild, moderate, and severe anxiety, respectively. Developed by Ors Robert L. Spitzer, Janet BW Williams, Kurt Kroenke, and colleagues, with an educational grant from Pfizer Inc. No permission required to reproduce translate, display or distribute.

PATIENT HEALTH QUESTIONNAIRE-9 (PHQ-9) Over the last 2 weeks, how often have you been bothered by the following problems? (Use"../" to indicate your answer). 1. A little interest or pleasure in doing things

Not at all

Several days

More than half the days

1 0 Feeling down, depressed or hopeless 1 0 Trouble falling or staying asleep or sleeping too much 0 1 Feeling tired or having a little energy 1 0 Poor appetite or overeating 1 0 Feeling bad about yourself-or that you are a failure or have let 0 1 yourself or your family down 7. Trouble concentrating on things, such as reading the newspaper or 1 0 watching television 8. Moving or speaking so slowly that other people could have noticed? 1 0 Or the opposite-being so fidgety or restless that you have been moving around a lot more than usual 9. Thoughts that you would be better off dead or of hurting yourself 1 0 in some way (For office coding: Total Score T .......

2. 3. 4. 5. 6.

Nearly every day

2 2 2 2 2 2

3 3 3 3 3 3

2

3

2

3

2

3

= ....... + ....... + ....... )

Scores of 5, 10, 15, and 20 represent cut points for mild, moderate, moderately severe, and severe depression, respectively. Developed by Ors Robert L. Spitzer, Janet BW Williams, Kurt Kroenke, and colleagues, with an educational grant from Pfizer Inc. No permission required to reproduce translate, display or distribute.

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PHYSICAL SYMPTOMS (PHQ-15) During the past 4 weeks, how much have you been bothered by any of the following problems?

Not bothered at all (0)

Bothered a little (1)

Bothered a lot (2)

a. Stomach pain b. Back pain c. Pain in your arms, legs or joints (knees, hips, etc.) d. Menstrual cramps or other problems with your periods (women only) e. Headche f.

Chest pain

g. Dizziness h. Fainting spells i.

Feeling your heart pound or race

j.

Shortness of breath

k. Pain or problems during sexual intercourse I.

Constipation, loose bowels, or diarrhea

m. Nausea, gas, or indigestion n. Feeling tired or having low energy o. Trouble sleeping (For office coding: Total Score T

=

+

)

PHQ-15 scores of 5, 10, and 15 represent cut points for low, medium, and high somatic symptom severity, respectively. Developed by Ors Robert L. Spitzer, Janet BW Williams, Kurt Kroenke, and colleagues, with an educational grant from Pfizer Inc. No permission required to reproduce translate, display or distribute.

I REFERENCES l. Wilson M, Roll J, Pritchard P, et al. Depression

and Pain Interference Among Patients With Chronic Pain After ED Encounters. J Emerg Nurs 2014 May; 40(3): e55-61. doi: 10.1016 j.jen. 2013.03.011. Epub 2013 Apr 28. 2. Chen Xi, Cheng HG, Huang Y, et al. Depression symptoms and chronic pain in the community population in Beijing, China. Psychiatry Res. 2012 Dec 30; 200 (2-3): 313-7. doi: 10.1016/j. psychres. 2012.04.013. Epub 2012 May 5. 3. Sarah EP Munce, Donna E. Gender differences in depression and chronic pain conditions in a national epidemiologic survey psychosomatics 2007;48(5):394-9.

4. Day MA, Thorn BE. The relationship of demographic and psychosocial variables to pain-related outcomes in a rural chronic pain population. Pain. 2010 Nov;151(2): 467-74. doi: 10.1016/j.pain. 2010.08.015. 5. Morasco BJ, Lovejoy TI, Lu M, Turk DC, Lewis L, Dobscha SK. The relationship between PTSD and chronic pain: Mediating role of coping strategies and depression. Pain. 2013 Apr; 154(4): 609-16. doi: 10.1016/j.pain.2013.01.001. Epub 2013 Jan 11. 6. Failde I, Duenas M, Agtiera-Ortiz L, et al. Factors associated with chronic pain in patients with bipolar depression: A cross-sectional study. BMC psychiatry 2013 Apr 15; 13: 112. doi: 10.1186/1471-244X-13-112.

Psychological Evaluation

7. Ambler N, Williams AC, Hill P, et al. Sexual difficulties of chronic pain patients. Clin J Pain 2001 Jun; 17(2): 138-45. 8. Green CR, Flowe-Valencia H, Rosenblum L, et al. Do physical and sexual abuse differentially affect chronic pain states in women? J Pain Symptom Manage 1999 Dec; 18(6): 420-6. 9. Roger D Weiss, Jennifer Sharpe Potter, Margaret L, et al. Reasons for opioid use among patients with dependence on prescription

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opioids: the role of chronic pain. Journal of Substance Abuse Treatment; April 2014. 10. Scott W, Trost Z, Bernier E, et al. Anger differentially mediates the relationship between perceived injustice and chronic pain outcomes. Pain 2013 Sep; 154(9): 1691-8. doi: 10.1016/j.pain. 2013.05.015. Epub 2013 May 14. 11. Arroll B, et al. BMJ Nov. 2003; pp. 1144-6. 12. Kroenke, et al. Annals of Int. Med 2007; 146: 317-25.

Chapter

17 Common Investigations in Pain Medicine Pankaj Surange

Physicians from wide-ranging disciplines such as anesthesiology, interventional pain physicians, physiatrist, neurology, internal medicine, orthopedics, and neurosurgery frequently encounter patients complaining of pain. Careful clinical correlation among the patient's history, physical examination, laboratory investigations and imaging studies may help physician identify the structures and processes responsible for the patient's symptoms. Diagnosing the cause of chronic pain and structures responsible for this pain is a big challenge. In such cases, diagnostic interventional blocks may help in differentiating the sources of pain. Laboratory Diagnosis

For those patients who have neuropathic pain, there is something wrong with how their nerves are transmitting messages. We have yet to come up with a diagnostic test that can show these nerve problems. Further complication arises in the chronic pain diagnostic process because pain is a multi-faceted issue. It can have a physical cause, but there are also emotional components to pain. The body's chemicals play a role, too. With such a complex mechanism, it is understandable that there would not be a single test that can accurately quantify pain. Complete hemogram is sent routinely in many cases, mainly when any infective or inflammatory condition is suspected as the causeofpain.Relevantblood tests are advised

if any associated chronic disease is suspected or to see their optimization. Blood tests are of importance in the diagnosis of specific forms of inflammatory arthritis. Blood tests are useful in confirming clinically suspected diagnosis and monitoring the disease activity. The tests should be used as adjuncts to a comprehensive history and physical examination. The value of a test in diagnosing a certain condition depends on its pretest probability. A positive test result with high pretest probability helps to make a diagnosis, but a negative test result with low pretest probability helps to rule out the diagnosis. However, clinicians cannot rely heavily on blood tests in making the diagnosis of rheumatologic diseases, except for certain tests that are highly specific for certain diseases. Improper application of these tests leads to misdiagnosis, inappropriate therapy, and unnecessary health care expenses. Many patients with early inflammatory arthritis who go on to develop severe chronic inflammatory rheumatic disease, such as rheumatoid arthritis (RA), psoriatic arthritis or ankylosing spondylitis, have normal blood tests when first seen. Acute phase reactants are proteins whose plasma concentration increases (positive acute phase proteins) or decreases (negative acute phase proteins) by at least 25% during inflammatory states. The effect of inflammatory molecules such as interleukin (IL)-6, IL-1, tumor necrosis factor a (TNF-a),

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interferon y(IFN-y), and transforming growth factor ~ (TGF-~) causes a change in hepatic protein synthesis collectively known as acute phase response. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are the most widely measured acute phase reactants in clinical practice.1 Measurement of the Acute Phase Response

The acute phase response develops in the setting of a wide range of acute and chronic inflammatory conditions: Severe bacterial, viral, or fungal infections; rheumatic and other inflammatory diseases; malignancy; and tissue injury or necrosis. These conditions elicit a response in which interleukin-6 and other cytokines trigger the synthesis by the liver of a variety of plasma proteins, including C-reactive protein (CRP) and fibrinogen. The detection and monitoring of this response can be clinically useful and is accomplished by measuring the level of CRP or by determining the erythrocyte sedimentation rate (ESR), which is influenced by the binding of fibrinogen to erythrocytes. As a general rule, CRP is a more sensitive and accurate reflection of the acute phase response than the ESR. C-Reactive Protein

CRP likely has a physiologic role in the innate immune response to infection and may participate in the clearance of necrotic and apoptotic cells. The availability of highly sensitive assays of CRP has allowed accurate determination of baseline CRP levels and has revealed a correlation between baseline CRP and cardiovascular disease. The median baseline level for young adults is 0.8 mg/L, and the 90th percentile is 3.0 mg/L. The baseline levels of CRP increase with age and with body mass index. Laboratories sometimes offer a choice between a routine CRP assay (suitable for the detection and monitoring of inflammatory disease) and a highly sensitive CRP assay for the determination of cardiac risk. During the acute phase response, levels of CRP rapidly increase up to 1000-fold, reaching

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a peak at 48 hours. With resolution of the acute phase response, CRP declines with a relatively short half-life of 18 hours. Because there are a large number of disparate conditions that can induce CRP production, an elevated CRP level does not have diagnostic specificity. An elevated CRP level, however, can provide support for the presence of a clinically suspected inflammatory disease, when other objective findings are absent. Values > 10 mg/L are generally thought to indicate clinically significant inflammation. Monitoring CRP levels can provide useful information on the activity of diseases such as rheumatoid arthritis and giant cell arteritis. Despite their apparent inflammatory nature, scleroderma, polymyositis, and dermatomyositis often elicit a little or no CRP response. CRP levels also tend not to be elevated in SLE unless serositis or synovitis is present. Elevations of CRP in the absence of clinically significant inflammation can occur in renal failure. Erythrocyte Sedimentation Rate

The ESR is determined by allowing anticoagulated blood to sediment for 1 hour in a glass tube (200 mm in length for the commonly used W estergren method; 100 mm for the Wintrobe method). Normal ranges for the ESR are 0-10 mm/hr and 0-15 mm/hr for men and women, respectively, but the upper limit of normal increases with age and with obesity. Because fibrinogen and certain other acute phase proteins (not including CRP) bind to erythrocytes and increase their sedimentation rate, the ESR is a measure of the acute phase response. The ESR responds slower ( over days) to the onset and resolution of an acute phase response than does the level of CRP, and the dynamic range of the ESR is less than that of CRP. More so than CRP, the ESR can be influenced by factors other than the acute phase response. The ESR is a useful diagnostic test when there is clinical suspicion of polymyalgia rheumatica or giant cell arteritis; it is also

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commonly used to monitor the activity of these conditions as well as that of rheumatoid arthritis. Due to the wide range of disorders associated with an acute phase response, elevations of the ESR have a little diagnostic specificity. Moreover, transient mild to moderate elevations can occur in the absence of other indications of disease. Marked elevations of the ESR (> 100 mm/hr by the Westergren method), however, are almost always due to a clinically significant condition, usually infection, malignancy, or rheumatic disease.2 The ESR is of very limited value in patients with the nephrotic syndrome or end-stage renal disease because virtually all have an elevated ESR (some > 100 mm/hr), probably due to high levels of fibrinogen. Elevations of the ESR in the absence of clinically significant inflammation also occur in pregnancy, anemia, erythrocyte macrocytosis, and hypercholesterolemia. Conversely, hypofibrinogenemia, polycythemia, microcytosis, sickle cell disease, and congestive heart failure lower the ESR. Autoantibodies

A variety of basic assays is used to detect autoantibodies. More than one type of assay may be available for any given autoantibody, and the particular test used may vary from institution to institution. In general, there has been a trend away from labor-intensive tests, such as agglutination assays and countercurrent immunoelectrophoresis, and toward assays amenable to automation, such as nephelometry and enzyme-linked immunosorbent assay (ELISA). Rheumatoid Factor

Rheumatoid factor is an autoantibody directed against the Fe region of IgG. The most commonly used methods of detecting rheumatoid factor are latex fixation (using latex beads coated with human IgG) and nephelometry (using human IgG as the target antigen). Both assays primarily detect IgM rheumatoid factors. The results of latex fixation assays are reported as the greatest dilution that retains

agglutination activity; in most laboratories, sera with titers of > 1: 40 are considered abnormal. Rheumatoid factor measured by nephelometry is quantified in international units, with 20 IU reported as abnormal in most laboratories. ELISAs for rheumatoid factor are also available but are not in wide use. ELISAs can measure IgG, IgA, and IgM rheumatoid factors. Associated conditions: Rheumatoid factor is present in 70-90% of patients with rheumatoid arthritis. Despite its name, rheumatoid factor is not specific for rheumatoid arthritis. Positive tests for rheumatoid factor occur in a wide range of autoimmune disorders, inflammatory diseases, and chronic infections. Also, the prevalence of positive rheumatoid factor tests increases with age; as many as 25% of persons over the age of 65 may test positive. In the absence of disease, the titer for rheumatoid factor is usually low (1: 160). High titer for rheumatoid factor (1: 640) almost always reflects an underlying disease. Interpretation of results: Because of the large number of disorders associated with rheumatoid factor, the value of a positive test for rheumatoid factor depends on the pretest probability of the disease. In the proper clinical setting a positive test provides strong support for the diagnosis of rheumatoid arthritis. However, it should be kept in mind that the combination of arthritis and a positive test for rheumatoid factor is not specific for rheumatoid arthritis and can be seen in patients with systemic lupus erythematosus (SLE), mixed connective tissue disease, systemic vasculitis, polymyositis, dermatomyositis, sarcoidosis, subacute bacterial endocarditis, and viral infections, particularly hepatitis C. A negative test for rheumatoid factor should not be the only reason to rule out the possibility of rheumatoid arthritis. From 10 to 30% of patients with long-standing disease are seronegative. At the time of presentation, however, the prevalence of a positive rheumatoid factor test is substantially lower (in the range of 50%). Therefore, the sensitivity

Common Investigations in Pain Medicine

of the test is lowest when the diagnosis is most likely to be in doubt. Antibodies to Cyclic Citrullinated Peptides

Proteins that contain citrulline are the target of an autoantibody response that is highly specific for rheumatoid arthritis. Citrulline, a neutral amino acid, is not genetically encoded. Citrullinated proteins arise through a posttranslational modification in which arginine residues are converted enzymatically to citrulline. Currently autoantibodies to citrullinated proteins are detected using ELISA with synthetic cyclic citrullinated peptides (CCP). Associated conditions: The presence of antiCCP antibodies appears to be quite specific for rheumatoid arthritis. The secondgeneration ELISA tests for anti-CCP antibodies (anti-CCP2) have a specificity for rheumatoid arthritis as high as 97%. The sensitivities of anti-CCP tests are in the range of 70-80% for established rheumatoid arthritis and 50% for early-onset rheumatoid arthritis. Thus, compared to rheumatoid factor, the currently available anti-CCP ELISA tests have superior specificity and comparable sensitivity for the diagnosis of rheumatoid arthritis. Most patients with rheumatoid arthritis are positive for both anti-CCP antibodies and rheumatoid factor, but some have only one of these autoantibodies, and others have neither. Interpretation of results: The presence of antiCCP antibodies provides strong support for the diagnosis of rheumatoid arthritis. Moreover, in patients with early-onset, undifferentiated, inflammatory arthritis, the presence of anti-CCP antibodies is a strong predictor of progression to rheumatoid arthritis and for the development of joint erosions. A negative test for anti-CCP antibodies does not exclude the possibility of rheumatoid arthritis, particularly at the time of initial presentation when approximately 50% of patients lack detectable anti-CCP antibodies.3 The specificity of the anti-CCP ELISA test suggests that this test will prove useful when

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determinations of rheumatoid factor are not. For example, initial studies indicate that antiCCP antibodies are not associated with chronic hepatitis C infection. In contrast to rheumatoid factor, therefore, testing for antiCCP antibodies may help to distinguish concomitant rheumatoid arthritis from viral arthritis in patients infected with hepatitis C. Antinuclear Antibodies

Antinuclear antibodies (ANAs) are autoantibodies directed against histones, double-stranded and single-stranded DNA, ribonucleoprotein (RNP) complexes, and other nuclear components. Current indirect immunofluorescence assays for ANA use Hep-2 cells, a human epithelial cell line, as the source of nuclei and are more sensitive than older tests that used rodent liver and kidney.4 Indirect immunofluorescence assays for ANA report the titer of the ANA and the pattern of nuclear staining. In most laboratories, ANA with titers 1: 40 are considered positive. The pattern of the ANA should not preclude, or substitute for, the ordering of more specific tests that are otherwise indicated. Associated conditions: Positive tests for ANA occur in wide range of conditions, including SLE and other rheumatic diseases, organspecific autoimmune diseases, lymphoproliferative diseases, and chronic infections. A number of drugs induce ANA, and less commonly, a lupus-like syndrome. Low titer ANAs are relatively common among healthy adults; in one analysis, an ANA titer of 1: 40 was seen in 32% of healthy adults and 1: 160 was seen in 5%. Interpretation of results: The sensitivity of the immunofluorescent ANA for SLE is very high (>95%). A negative result, therefore, is very strong evidence against this diagnosis and usually precludes the need to pursue tests for antibodies to specific nuclear antigens (e.g. dsDNA, Sm, or RNP). A positive ANA test is one of the diagnostic criteria for drug-induced lupus and mixed connective tissue disease. The sensitivity of the ANA for scleroderma is >85%.

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In general, the probability of an underlying autoimmune disease increases with the titer of the ANA. Nonetheless, because the specificity of the ANA is limited, the value of a positive test depends on the pretest probability of disease. In the proper clinical context, a positive ANA by immunofluorescence provides supportive evidence of disease and should prompt tests for antibodies to specific nuclear antigens. Serial determinations of ANA by immunofluorescence are not useful for monitoring disease activity. Summary

• ESR and CRP are markers of inflammation and are elevated in inflammation. ESR can be elevated without inflammation in hypergammaglobulinemia or anemia. • CRP is a more sensitive marker of inflammation and is independent of factors affecting ESR. • Many patients with active lupus do not have elevated CRP levels; elevated CRP can suggest bacterial infection. • ANA testing is very useful in establishing a diagnosis of SLE. Nearly all patients with lupus have a positive ANA (sensitivity is 93-95%, but specificity is 57%). However, most patients with positive ANA do not have lupus, because the prevalence of lupus is low in the general population. • ANA titer is not used for assessing the disease activity in lupus. Thus, serial ANA testing is of unknown value. • Anti-DNA antibody testing is very useful in the diagnosis of SLE and is also a useful biomarker of SLE disease activity. • Anti-Scl-70 antibody is very useful in diagnosing systemic sclerosis and anticentromere antibody in diagnosing limited scleroderma. Anti-Scl-70 and anticentromere antibodies rarely coexist in the same patient. • SSA and SSB antibodies should be checked in patients with sicca symptoms. Patients with primary Sjogren' s syndrome with SSA or SSB antibodies represent the most clinically and immunologically active subset.

These patients need very close follow-up for development of extraglandular features. • The sensitivity of rheumatoid factor for rheumatoid arthritis is around 50-80% and specificity is 85-90%. It may be negative in the early stages of rheumatoid arthritis, and positivity increases over time. • Between 70 and 90% of patients with Wegener's granulomatosis test positive for ANCAs in the c-ANCA pattern, with antibodies directed against PR3. A negative ANCA assay does not exclude Wegener's granulomatosis. • Between 40 and 80% of patients with microscopic polyangiitis are ANCA positive and usually have the p-ANCA pattern with MPO specificity. • The role of sequential ANCA titers after the diagnosis is established is unclear. A recent study showed a weak association between disease activity and ANCA levels. Recently screening blood panel to evaluate chronic pain patients has been introduced. Recommended here is based on the knowledge that severe chronic pain produces inflammation and stimulatory or suppressive effects on the pituitary-adrenal-gonadal axis.5-7 Recommended blood panel in a new chronic pain patient: • AM cortisol • AM pregnenolone • Erythrocyte sedimentation rate (ESR) • C-reactive protein • Total testosterone. Four of the blood tests in the panel are based on chronic pain's major effects on the adrenal gland and the inflammatory response. Testosterone is the hormone in males and females that often is lowered with even low dosages of a weak opioid. Severe chronic pain, per se, may also have an adverse effect on testosterone blood levels. Although pain's effect on the pituitaryadrenal-gonadal axis is well known, it is somewhat uncertain as to how pain causes an inflammatory response and an elevation of the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Although some

Com m on Investigations in Pain Medicine

underlying cause of pain such as rheumatoid arthritis or hepatitis may cause a serum elevation of the ESR and CRP, it appears that a pain site unrelated to any underlying disease may cause the ESR and CRP to elevate. It is now documented that the ESR will be elevated in uncontrolled pain and will normalize when pain control is achieved. Uncontrolled pain causes a stress-type release of pituitary adrenocorticotrophin hormone (ACTH) which overstimulates the adrenal gland to raise serum levels of cortisol and other adrenal hormones including catecholamines. It is for this reason that pulse rates and blood pressure may rise in a pain flare or with chronic, uncontrolled pain. If serum pregnenolone is low, it is assumed that production of all adrenal-produced glucocorticoids and androgenic and estrogenic compounds are reduced since pregnenolone is the precursor of all these compounds. Cortisol levels less than one indicate severe adrenal exhaustion which can result over time from excess adrenal stimulation. Levels less than 1.0 µg/ dl are often not compatible with life, so this patient is extremely ill and requires vigorous pain control. The low adrenal and testosterone levels certainly provide an explanation for fatigue and weakness. Ultrasound as Diagnostic Tool in Musculoskeletal Disorders

For diagnostic ultrasound, recent advances in technology have improved ultrasound's

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ability to detect a myriad of musculoskeletal problems with enhanced resolution. Early detection of erosive disease, assessment of synovial tissue, assessment of effusions, detection of enthesitis in seronegative spondyloarthritis, assessment of treatment response, assessment of crystal arthropathy, needle guidance in aspiration, injection and biopsy are the areas where ultrasound is of definite advantage over other modalities.8 Diagnostic ultrasound also can examine larger areas with extended field of view where patient can direct towards symptomatic area and the clinician can focus the examination of most relevant area. Ultrasound also has the advantage of being a dynamic study, allowing physicians to observe pathological movements in tendons, bursa, ligaments, muscles or joint in real time. Inflammatory Arthritis

Ultrasound (sonography) aids in the confirmation of synovitis in early inflammatory arthritis.9 The sonographic evaluation of inflammatory arthritis has been aided by consensus definitions of synovitis and erosions by the OMERACT group.l? Small amounts of fluid can be detected in joints as well as tendon sheaths (Fig. 17.lA). Ultrasound is also more sensitive in the detection of enthesitis. Increased vascularization can be demonstrated by power Doppler (Fig. 17.lB). Ultrasound is more sensitive than plain X-rays in the detection of erosions. The earlier

Figs 17.1A and B Detection of effusion in the volar recess of the PIP joint-longitudinal and transverse views

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Fig. 17.2 Longitudinal view of the wrist revealing active synovitis

Fig. 17.4 Supraspinatus tendon with faint hypoechoic linear subacromial bursa (arrow) and overlying deltoid muscle

detection of erosions may lead to adjustment of remittive therapies especially in the presence of active synovitis. In a patient with established inflammatory arthritis, sonography may be useful in documenting ongoing synovitis.l! Although the traditional view of inflammatory arthritis has been mainly to follow joints, disease activity may also affect the tendon and tendon sheaths. Similarly, sonography can be readily used at the bedside to evaluate nerve entrapment at sites such as the carpal or cubital tunnel. The hallmark prestenotic dilation may be demonstrated.

(" double contour sign") while chondrocalcinosis is detected within the cartilage.12 Sonography is more sensitive than plain X-rays in detecting erosions. It is also a sensitive tool in the detection of tophi13 (Figs 17.3A and B). Technical factors that affect US include artifacts that can mimic real pathology. Ultrasound involves the reliance of placing the transducer and hence the beam at a 90° angle to the structure being imaged.14 Any deviance from this will result in the reflection of the beam away from the transducer, causing a reduction in the echogenicity (brightness) of the tissue being examined. This artifact is referred to as anisotropy and can be eliminated by maintaining the beam perpendicular to the involved tissue (Figs 17.SA and B). Good

Crystalline Arthropathy

Sonography can differentiate deposition of urate on cartilage from chondrocalcinosis. Urate deposits on the surface of the cartilage

Figs 17.3A and B Tophaceous gout and double contour sign at first metatarsophalangeal joint

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Figs 17.SA and B (A) Transverse view of the proximal long head of the biceps in the bicipital groove; (B) Same image as in (A). Now the transducer is not 90° to the tendon, causing it to appear hypoechoic (darker). This may mimic a tear of the

tendon and is referred to as anisotropy

technique also involves maintaining adequate skin contact, confirming the presence of pathology in orthogonal planes, and using the appropriate transducer size for the specific situation. Tendon and Ligaments Pathology

The evaluation of tendon pathology is probably the most common clinical indication to obtain a diagnostic musculoskeletal ultrasound. On US, normal tendon, which is composed of fascicles of collagen fibers running in parallel, appear as fibrillar hyperechoic (brighter) bands. In normal conditions, there will also be a flat hypoechoic structure surrounding the tendon, representing a synovial sheath containing a small amount of fluid.15 An exception to this is the Achilles tendon, which has a closely adherent paratenon and is often normally imperceptible. In cases of tenosynovitis, there will be an increase in synovial sheath fluid indicative of underlying inflammation. Exceptions do exist. A significant amount of fluid surrounding the biceps may indicate primary bicipital tendonitis. However, fluid around the biceps tendon may be a secondary sign of a complete rotator cuff tear as fluid communicates with the glenohumeral joint through the subacromial bursa.

Joints

Though plain radiographs and MRI are useful at assessing intra-articular and periarticular pathology, US can add a complementary role for these imaging modalities.16 For example, US is undeniably the best imaging modality for detecting small joint effusions, which are indicative of underlying joint pathology. In fact, effusions as small as one ml can be identified with diagnostic US17 (Fig. 17.6). With these small effusions it may be difficult

Fig. 17.6 Normal appearing longitudinal view of the

hypoechoic (dark) suprapatellar bursa (arrow) underlying the quadriceps tendon. The patella is the hyperechoic white structure to the left and the femur is the hyperechoic structure towards the bottom of the image. An effusion would be visible in this location

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to blindly aspirate the joint. In these cases, US helps not only to locate the presence of an effusion but also serves as a guide for aspiration. SPINE IMAGING

Familiarity with both anatomy and radiologic anatomy of the spine is a prerequisite to understanding the various disorders and pathologies that affect the spine and its components. X-ray

Image formation with X-rays depends on a differential attenuation between tissues. The extent of this differential determines the amount of contrast between different tissues in the image formed. Density is one of the most important factors affecting attenuation, and radiographic image contrast is largely dependent on differences in tissue density (Fig. 17.7). Intervertebral discs are not visible on X-rays but their height can be estimated between intervertebral spaces. The AP view of the dorsal and lumbar spine shows the pedicles at each side of the vertebral bodies.

Fig. 17.7 Plain X-ray showing the difference between the compact "white" cortical bone surrounding the trabecular spongy bone vertebral body as a thin pencil-like white line (downward arrow) and the lower density that appears grayish

The pedicle size and shape as well as the interpedicular distance might point to a possibility of intraspinal space-occupying lesion (SOL).

Figs 17.SA and B Plain X-rays of the cervical spine. (A) Air within the trachea appears as a dark structure (between the arrows) superimposed on the cervical spine in an AP projection; (B) Intestinal contents and air bubbles are superimposed on the lumbar spine in an AP view

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Figs 17.9A and B X-ray-AP and lateral: (A) The interpedicular distance measured on the thoracolumbar AP projection indicates the transverse width of the spinal canal. This distance increases gradually in the craniocaudal direction; (B) The sagittal diameter of the spinal canal can be measured on the lateral projection by measuring the distance between the posterior aspects of the vertebral body and the spinolaminar line

Their erosion might indicate a metastatic disease. Ossification of the posterior longitudinal ligament (OPLL) and diffuse idiopathic skeletal hyperostosis (DISH) can be easily recognized in the lateral view.

Oblique Views

Clearly show the "Scottie dogs" (Fig. 17.lOA). The "nose" represents the transverse process, the "forelimb" the inferior articular process, the "ear of Scottie dogs " the superior articular process, the "body" the lamina, and the "face"

Figs 17.10A and B Plain X-ray (oblique view) demonstrating the Scottie dogs

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the pedicle and "eye" the junction of transverse process and superior articular process. Special attention should be devoted to the "dog's neck," which is the pars interarticularis. A break in this region exists in up to 6% of the population and is called spondylolysis. Should the break occur bilaterally, it may compromise the stability of the spine and lead to vertebral slippage called spondylolisthesis. The upper lumbar facet joints are oriented mostly in the sagittal plane, whereas the lower facets are oriented more coronally. In the cervical spine the pedicles are obliquely oriented anteroposterior mediolaterally so that the intervertebral foraminae will be exposed only in oblique projections. (Fig. 17.lOB). Oblique views of the cervical spine will therefore demonstrate the pedicles, intervertebral foraminae, and the uncovertebral joints and facets. Lateral view of cervical spine provides an excellent view of the odontoid process and its relationship to the anterior arch of the Cl vertebra (Figs 17.llA and B). The distance between the two should not exceed 3 mm in an adult and 5 mm in a child. On an AP view the odontoid process could be clearly seen only in an open mouth view.

Pathologies on X-ray

Herniated discs cannot be seen in plain films. When they herniate through the vertebral endplate, however, a situation that is frequently seen and believed to be secondary to endplate injury, they become visible. These herniations are called Schmorl's nodes (Fig. 17.13). They are commonly seen in spinal X-rays as small circumscribed end plate defects that are continuous with the discs (Fig. 17.12).

Fig. 17 .12 Anterior Schmorl's node on the upper endplate of

L4 in a lateral plain film of the lumbar spine

Figs 17.11A and B Plain films demonstrating the atlantoaxial complex. (A) Lateral projection allows measurements of the distance between the odontoid and the anterior arch of C1 (arrows). (B) Open mouth view demonstrating the relation between the odontoid and the lateral masses of the first cervical vertebra, the atlas

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Compression Fractures

The 'three-column model' (see previous page) can be used to form a basic classification of thoracolumbar spinal injuries. This page also discusses osteoporotic fractures, and fractures of the transverse and spinous processes. Spinal injuries which are seen to disrupt structures of 2 or more columns are considered 'unstable'. If the middle column is seen to be injured it is usually taken that another column must be injured even if no anterior or posterior column fracture is visible. If an injury is seen which disrupts 1 column then a second fracture is also present in approximately 15% of cases. If a two-column injury is seen then likelihood of a second fracture increases to 40%. Fig. 17.13 X-ray image of Schmorl's nodes in the lumbar spine

As the disc degenerates, nitrogen gas may accumulate within the disc and can be seen on X-rays. The accumulation of gas within the substance of the disc is referred to as the "vacuum phenomenon" and is most prevalentin the lower lumbar discs (L4-L5-S1) and occasionally in the lumbar facet joints (Fig. 17.14).

1 Column-Anterior Compression Injury

Anterior compression injury is a common fracture pattern which results from traumatic hyperflexion with compression. Although considered 'stable' the greater the loss of height anteriorly the greater the risk of middle column involvement. X-ray may underestimate

Degenerated disc with vacuum phenomenon

Fig. 17.14 Vacuum phenomenon in a degenerative lumbar disc, in a plain film

Fig. 17.15 Anterior compression fracture-lumbar spinelateral. Poorly defined dense (white) fracture line is visible with a detached fracture fragment. L 1 has lost height anteriorly and there is disruption of the anterior column only

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of vertebral body fracture fragments into the spinal canal leads to a high-risk of spinal cord or nerve root damage. 3 Column-Flexion-distraction Fracture

Flexion-distraction injuries are associated with high force deceleration injuries and are most common at the thoracolumbar junction. Also known as 'Chance-type' fractures (after the radiologist who first described them) these injuries are unstable and carry a high-risk of neurological deficit and abdominal organ injury. The 'fracture' line may pass through the disc rather than the vertebral body, and so there may not be visible bone injury of the anterior column (Fig. 17.18). Osteoporotic Fractures Fig. 17.16 Anterior compression injury-lumbar spine-AP. Loss of vertebral body height can be seen but the fracture is not visible on AP view

the extent of injury and so if there has been high-risk injury or other suspicion of instability then CT should be considered.

Thoracolumbar spine injuries are very common in patients with osteoporosis. Common fracture patterns include 'wedge' injuries and 'biconcave' fractures (Figs 17.19A and B). Spondyloarthropathy

'Burst' fractures result from high force vertical compression trauma. Posterior displacement

Initially, enthesopathic changes, erosions followed by sclerosis, appear at the corners of the vertebral bodies and lead to squaring of

Fig. 17.17 Thoracolumbar 'burst' fracture-lateral. Both the anterior and middle columns are disrupted. A large vertebral body fragment is displaced anteriorly

Fig. 17 .18 Flexion-distraction/'chance' fracture-lateral. All three columns are disrupted

2 Columns-'Burst' Fracture

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Figs 17.19A and B (A) Thoracic spine-'wedge' compression fracture; (B) Lumbar spine-'biconcave' fracture

the vertebrae. These changes can be easily detected on plain films (Fig. 17.20). Erosions and whiskering appear in the sacroiliac joints and in the pubic region (Fig. 17.21). Initially, widening of the sacroiliac joint space occurs and later on blurring of the sacroiliac joint margins will be seen. Over the course of months or years the sacroiliac joints will fuse. Subsequently ossification of the vertebral

Fig. 17.21 AP plain film of the lumbosacral region. Fusion of the sacroiliac joints and facet joints is seen. Note the calcification of the supraspinous ligament, which is bridging the spinous processes

bodies and the annulus pulposus leads to the formation of thin syndesmophytes. They form bridges between the vertebral bodies, eventually leading to spine fusion. CT SCAN

Fig. 17.20 Lateral plain X-ray of the thoracolumbar spine. Straightening of the spinal column and loss of the normal lordosis are apparent. Squaring of the vertebral bodies with sclerosis at the vertebral corners is visible

Computed tomography (CT) is a technology using ionizing radiation to generate images resulting from differential X-ray absorption of the specific tissues examined. CT produces cross-sectional displays and, multidimensional 2D and 3D reconstructions and therefore, offers a well-accepted high degree of clinical capability and utility for examining the spine.

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Fig. 17.22 Lateral plain film of the lumbar spine showing a "bamboo spine." Ossification of the anterior longitudinal ligament is seen (arrow) bridging all the vertebral bodies across the discs. Note that the facet joints are fused as well

Fig. 17.23 Cervical spine plain film in a patient with AS. Note the calcification of the anterior longitudinal (arrow) and posterior longitudinal ligaments, and fusion of the facet joints with preservation of the disc spaces

Depending on the nature of the disorder, CT may be the primary modality used or it may complement other modalities such as radiography, magnetic resonance (MR), ultrasound (US) or nuclear imaging studies. The strength of CT lies in the detailed depiction of bone and, therefore, it has greatest utility in evaluating the bony spine, as opposed to the spinal cord or other soft tissue structures.

radiographs of a spinal segment (cervical, thoracic, lumbar, and/ or sacral spine) are abnormal, equivocal, or nondiagnostic following a traumatic event. CT can be used for evaluating vertebral compression/ insufficiency fractures in both acute and chronic clinical situations.18 2. Degenerative conditions and osteoarthritis evaluation. CT is often used to study the spine for conditions such as lumbar stenosis or in evaluating degenerative disc disease, and is the primary evaluation technique when MRI is contraindicated (e.g. the presence of cardiac pacemaker or other implants that are not MRI compatible ).19-21 a. Neoplastic conditions and their complications. CT can provide valuable information in the evaluation of primary or metastatic neoplasms of the spine, to include marrow-replacing conditions such as multiple myeloma. It can also provide valuable information in relation to complications of neoplastic disease,

Primary indications for CT of the spine include, but are not limited to

1. Traumatic injuries, including evaluation of acute injuries and their potential chronic/long-term reparative changes. CT of the spine is particularly useful in and is considered a primary imaging evaluation of acute spine trauma in adults. However, given that the vast majority of cervical spine injuries in young children are of soft tissue rather than bone, it should be recognized that the use of CT in this population is of limited utility. If there is a clinical concern for spinal injury, MRI should be considered in pediatric patients. CT may be used when

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Fig. 17.24 Axial CT cut through a lumbar vertebra showing the difference between dense compact cortical bone and the trabecular bone. Note the Y-shaped basivertebral venous plexus within the vertebral body

including misalignment and pathologic vertebral compression fractures. 22, 23 b. Abnormalities related to alignment or orientation of the spine, such as scoliosis or spondylolysis with or without spondylolisthesis. Traditional CT study of the spine consists of multiple slices traversing the spinal elements in axial plains, perpendicular to the long axis of the spinal column, along its different curvatures-the cervical and lumbar

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lordosis and the dorsal and sacral kyphosis. The slice thickness can be chosen to fit the desired resolution. It can go down to less than 1 mm in width, especially when multiplanar reconstructions (MPRs) are desired or needed. A smaller slice width will usually achieve better resolution, down to a certain limit. Modern CT systems can produce volumetric images so that reconstructions can be produced through the whole volume at any desirable plane with reasonable and good contrast resolution. True sagittal and coronal images through the spine can be produced and enable evaluation of the alignment of the vertebrae and comparison of their shape and size, as well as evaluation of the width and shape of the spinal canal (Figs 17.26A and B). Contrast agents can be used with CT studies in two fashions: 1. Intravenous injection of contrast material is indicated when pathologies such as primary or secondary tumors, or inflammatory processes are looked for, as they can enhance pathologic soft tissues within the bones or inside the spinal canal. 2. Intrathecal injection of contrast agents into the subarachnoid space is performed by a spinal tap to perform CT-myelography.

Figs 17.25A and B Axial image: (A) Through the disc and through vertebral body; (B) Exiting nerve roots can be seen in intervertebral foramen (arrows)

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Figs 17.26A and B (A) Sagittal CT reconstruction of the dorsal spine. Sagittal diameter of the spinal canal and the discs height can be more accurately measured and the end plates of the vertebral body are better assessed than on X-rays; (B) Three-dimensional reconstruction of the cervical spine including vertebrae, adjacent soft tissues, and the major blood vessels

Discography

Provocative discography is an imagingguided procedure in which a contrast agent is injected into the nucleus pulposus of the disc. Despite its controversial history, it remains the only imaging technique that provides both anatomical and functional information about a diseased disc. Disc morphology is usually assessed on either radiographs or computed tomography (CT), or both. Functional evaluation of the disc consists of pain provocation and careful assessment of the patient's response to pain. As provocative discography is an invasive procedure, it should not be used as a screening study in patients with back pain. It should instead be reserved for carefully selected patients whose painful symptoms cannot be explained by findings on non-invasive imaging modalities such as magnetic resonance imaging or CT, and who are not responsive to conservative measures.

Despite an incomplete understanding of the pathophysiology of discogenic pain and the variable pain response of individual patients, 16 many studies have supported provocative discography as a valuable diagnostic test in the investigation of discogenic pain. Specific indications for provocative discography are: 1. Further evaluation of a radiologically abnormal disc for the full extent of abnormality or correlation of the abnormality with the clinical symptoms. 2. Investigation of persistent, severe symptoms that do not correlate with equivocal or inconsistent MR imaging or CT findings. 3. Determination of symptomatic disc levels in cases where MR imaging or CT shows disc disease at multiple levels. 4. Assessment of disc prior to fusion to determine if a disc within proposed fusion

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segment is symptomatic, and whether the adjacent discs are normal. 5. Assessment of disc prior to percutaneously directed therapies such as intra-discal electrothermal therapy. 6. Assessment of patients prior to minimally invasive surgery in order to confirm that disc herniation is contained, or to investigate contrast distribution before chemonucleolysis. 7. Assessment of post-surgical failed back syndrome of patients in whom MR imaging is non-diagnostic, including differentiating recurrent disc herniation from a painful pseudoarthrosis or identifying asymptomatic disc within a posteriorly-fused segment. CONTRAINDICATIONS

Contraindications to provocative discography are: 1. Patients with a known bleeding disorder and those on anticoagulation therapy. 2. Pregnancy.

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3. Systemic infection or skin infection over the puncture site. 4. Severe allergy to injectate, especially the contrast agent. 5. Previously-operated disc. 6. Solid bone fusion that does not allow access to the disc. 7. Severe spinal cord compromise at disc level to be investigated. Interpretation

Disc morphology is usually determined on evaluation of anteroposterior and lateral radiographs obtained after intradiscal contrast injection (Figs 17.27A and B). A normal disc maintains a normal height on both AP and lateral radiographs. Injected contrast agent remains in the nucleus pulposus, and may be unilocular ("cottonball" or rectangular) or bilocular ("Hamburger bun") in shape. Sometimes, a Schmorl' s node is seen as focal protrusion of injected contrast agent into the adjacent vertebral endplate.

Figs 17.27 A and B Discographic patterns: (A) Anteroposterior; (B) Lateral radiographic projections show a normal bilocular

L2/3 disc

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In degenerated discs, discography shows a reduced disc height, and complex or multiple irregular fissures in the annulus fibrosis, with or without contrast leakage through annular tears. A bulging disc is often associated with degeneration, and is characterized by circumferential, diffuse and symmetrical annular bulging. Discography may show annular fissures with an intact peripheral annulus. Disc protrusion refers to focal, often asymmetrical, central or posterolateral protrusion of disc material within an intact posterior longitudinal ligament. There is small posteroinferior tear of the L3/4 disc. The L4/5 disc is decreased in height, and had extensive annular disruption and posterior protrusion. CT discograms are CT images obtained following discography (Fig. 17.28). It provides excellent anatomical details in the axial plane. The Dallas discogram description (DDD) is based on CT appearances and was originally classified into grades Oto 3, later modified to four grades.

Figs 17.28A to D CT discographic patterns: (A) Axial CT image shows a normal L3/4 disc (DDD grade O); (B)Axial CT image shows a small L4/5 posterior annular tear (ODD grade 3); (C) Axial CT image shows extensive L5/S1 posterior annular disruption (DDD grade 4 ); (D) Sagittal reconstructed CT image provides a good overview of a normal L3/4 disc, and posterior tears of protruding L4/5 and L5/S1 discs

Grade 0: Contrast agent is confined entirely within the normal nucleus pulposus (Fig. 17.28A). Grade 1: Contrast agent extends radially along fissure involving the inner one-third of the annulus fibrosis. Grade 2: Contrast agent extends into the middle one-third of the annulus fibrosis. Grade 3: Contrast agent extends into the outer

one-third of the annulus fibrosis, either focally or radially, to an extent not greater than 30° of the disc circumference (Fig. 17.28B). Grade 4: Contrast agent extends into the outer

one-third of the annulus fibrosis, dissecting radially to involve more than 30° of the disc circumference (Fig. 17.28C). Further modifications of the DDD are: Grade 5-representing a full-thickness tear,

either focal or circumferential, with extraannular contrast leakage.

Fig.17.29 Pictorial diagram showing post discography CT scan modified Dallas grades. Grade 0-normal disc, cotton-ball appearance. Grade 1-radial tear up to inner one-third of annulus fibrosus (af), Grade 2-radial tear up to middle one-third of af, Grade 3-radial tear up to outer one-third of af, but extends 30° of disc circumference, Grade 5-radial tear with extra-annular leakage into epidural space

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Degenerative Spine

Fig. 17.30 Vacuum phenomenon in a CT scan of a lumbar disc. Sign of disc degeneration

Fig. 17.32 Axial CT slice of a lumbar vertebra. Note the obliterated lateral recess due to the severe stenosis. Facet arthropathy with vacuum phenomenon in both facet joints is noted

scan, however, which can detect as of bone turnover (i.e. bone deposition even before the actual fracture has developed), may be positive and thus is an important diagnostic tool at the early stages of the condition. Single photon emission computed tomography (SPECT) may be the most sensitive test for detecting impending pars defects, as bone under stress with increased osteoblastic activity due to remodeling will have increased activity and appear hot. Later on, when the defect is established and is large enough, it can be spotted on various projections on plain films (Fig. 17.33).

Fig. 17.31 Axial CT slice demonstrating severe narrowing of the spinal canal in both the sagittal and coronal diameters. Note the severe !re-foil shaped stenosis of both lateral recesses (arrows)

Spondylosis

In the initial stages, when the fracture is forming, the plain films may be negative. Bone

Fig. 17.33 Axial CT image showing bilateral bony defects (arrows). Note that the sagittal canal diameter is elongated

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CT scan is the most sensitive method for detection of spondylolysis, whether it is unilateral or bilateral. The defects can be easily spotted in an axial cut. Spinal Infections

Plain radiographs have a very low sensitivity and specificity in the initial stages of infection and thus are unreliable and do not exclude spinal infection when they are found to be normal. CT scan is more sensitive than plain radiographs but is not specific enough and thus is not as helpful as MRI. It will show disruptions in the vertebral cortex and erosions in the vertebral bodies. The erosions will be irregular and darker (hypodense) than healthy bone. In tubercular osteomyelitis, CT examination will clearly show vertebral body erosions, destruction, and sequestration (depending on infection duration). Bone fragments may appear within the spinal canal or in the soft tissues (Figs 17.34A and B). CT with contrast may help delineate the soft tissue abscesses. The abscesses may be prevertebral, paravertebral, or epidural.

Spine Fractures

When the posterior part of the vertebral body is involved, it becomes essential to rule out involvement of posterior cortex. Burst fractures are clinically significant because they may be associated with a retropulsed fragment-a bone fragment that is pushed posteriorly into the spinal canal-leading to neurological compromise (Figs 17.35A and B). MRI FOR SPINAL IMAGING

MRI is an image modality based on an interaction between radiofrequency (RF) waves and hydrogen nuclei under the influence of a strong magnetic field. Two main types of magnets are currently used in clinical imaging: Superconductive magnets and permanent magnets. Their field strength is measured in Tesla, which is a unit of magnetic field strength that is equal to 10,000 Gauss. Under the influence of the strong magnetic field of the MR system, the hydrogen nucleus processes at its own resonant frequency-the Larmor frequency, derived from its gyromagnetic ratio (a fundamental characteristic) and linearly related to the field strength.

Figs 17.34A and B (A) Axial and (B) Sagittal reformatted CT cut through the thoracic spine shows extensive destruction of 3 consecutive vertebral bodies affected by TB. Note the penetration of the infective material through the anterior and posterior cortex into the retroperitoneal soft tissues and into the vertebral canal respectively

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Figs 17.35A and B CT showing a burst fracture with a retropulsed segment into the spinal canal (arrows). The posterior vertebral wall (middle column) has been fractured, and a large bony segment is compromising the spinal canal

Radiofrequency waves tuned to the Larmor frequency are transmitted repeatedly to the body being imaged for very short fractions of time measured in milliseconds. These bursts of energy are called RF pulses. Having the same frequency, the RF pulses can stimulate the hydrogen nuclei. Following the RF pulse the stimulated hydrogen nuclei tend to go back to the lower energy state and "relax" by two mechanisms. The first is termed Tl relaxation and the second T2 relaxation or T2 decay. An electrical

signal is then received by an antenna-the receiving coil. All the signals derived from the volume imaged are then organized by the gradient coils to form an image.24, 25 Different tissues have different Tl and T2 relaxation times under the same magnetic field. The differences in the relaxation times of different tissues are the key to the excellent contrast among them on the MR image created (Figs 17.36 to 17.38). To date MRI is the only imaging modality that has the ability to demonstrate and

Figs 17.36A and B Sagittal T1 and T2 (FSE) MR images of the lumbar spine. (A) On T1WI the discs appear darker, of lower intensity than the vertebral bodies. Their texture appears homogenous on T1WI; (B) On fast T2WI the normal discs (nucleus pulposus) are of higher intensity than the vertebral bodies. The annulus fibrosus is darker (star) as shown at L4-5 level and above. The disc at L5-S 1 level is totally dark due to degenerative changes. Note the normal brightness (high intensity) of the CSF within the dural sac, similar to the fatty tissue in the epidural space

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Figs 17.37A and B MR images of the lumbar spine, in axial views through the intervertebral foraminae at a level below the conus medullaris. The nerve roots (cauda equina) are located in the back of the dural sac. They appear (A) gray but brighter than CSF on T1-weighted images; (B) Dark in contrast to the high intensity of the CSF on T2WI

Figs 17.38A and B Sagittal MR images of the lumbar spine through the intervertebral foraminae. (A) The fat within the foramen is of high intensity on the T1-weighted image. It provides a bright background to the low intensity of the exiting nerve root. Note the radicularveins in the lower-third of the foramen; (B) On sagittal T2WI through the lateral recesses, the obliquely oriented nerve roots are demonstrated on their course toward the intervertebral foraminae

delineate clearly all spinal components and, is therefore, considered the best imaging modality of the spine.

Tl -weighted images (Tl WI) are used for tissue discrimination. T2-weighted images (T2WI) are very sensitive to the presence of

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increased water and to differences in susceptibility between tissues. Usually both Tl WI and T2WI are used in routine spinal imaging. Frequently used techniques in spinal imaging are fat suppression (STIR) and CSF suppression (FLAIR). The former technique is used in order to suppress the fat signal of the bone marrow, and the latter suppresses the high/bright signal deriving from the CSF, inverting it dark in T2-weighted sequences. Contrast MRI

The most common contrast agent used in MRI studies is gadolinium DTPA. Gadolinium is an earth element and a paramagnetic substance that causes shortening of Tl on the image. Its effect on T2 is negligible. It is injected intravenously in a peripheral vein, flows with the bloodstream, and accumulates in specific normal tissues of the spine such as the red bone marrow, dura, and blood vessels. It accumulates in pathological conditions such as lesions where the blood-brain barrier is absent or at a point of breakdown within the cord, in fibrous tissue within disc fissures, postsurgical scar tissue, and abnormal bone marrow infiltrated by primary or secondary tumors or affected by hematological disorders. Because shortening of Tl brings about higher signal intensity on a Tl WI, areas of gadolinium accumulation enhance; that is, they appear bright. To better depict these enhanced pathologies, a Tl WI without contrast must precede that with contrast. The changes can then be assessed. Fat suppression can also help differentiate a bright enhancing lesion from normal bright fat.

Fig.17.39 L2-3 degenerated disc (arrow), where the annulus and nucleus pulposus have the same dark signal

Fatty bone marrow infiltration occurs during the aging process, resulting in brighter vertebral signal whereas the disc signal becomes darker and more homogenous. The end result of this degenerative process is a "black disc," where the annulus and nucleus have the same dark signal (Fig. 17.39).

DISC PATHOLOGIES Disc Degeneration

On Tl -weighted images the signal of the nucleus and the annulus may look alike and also resemble the vertebral body signal. In healthy discs the nucleus pulposus and the annulus fibrosis can be easily differentiated using T2weighted images: The nucleus pulposus appears brighter than the annulus fibrosus (Fig. 17.39).

Fig.17.40 Type I: Low signal in T1-weighted sequences and high signal in T2 indicating edema (arrows)

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Fig. 17.41 Type II: High signal in T1-weighted sequences and either high or intermediate signal in T2 indicating fatty replacement (arrows)

Over time, disc degeneration leads to abnormal loads that result in degenerative changes in the endplate region. These are called "Modic changes".

Fig. 17.42 Type Ill: Low signal in T1 and low signal in T2-sclerotic changes (arrows)

Internal Disc Disruption

Annular tears initially appear on MRI as highintensity zones (HIZs) on T2-weighted images. These can be easily seen on sagittal and axial MRI cuts as small areas of increased signal and are usually found in the posterior or posterolateral aspects of the annulus (Fig. 17.43). The current histological study indicated that the HIZ in the patients with low back pain represented the ingrowth of the

vascularized granulation tissue into the tears in the posterior part of the painful disc.26-29 Defined as localized disruption of the disc annulus which extends: Radially-disruption of annular fibers extending from the nucleus outward toward the periphery of the annulus, usually in the vertical (craniocaudal) plane, with occasional horizontal (transverse) components.

Figs 17.43A and B (A) Sagittal T2-weighted magnetic resonance image (MRI) showing a high-intensity zone (arrow) within the posterior annulus at L4-5; (B) Axial T2-weighted magnetic resonance image (MRI) showing a high-intensity zone (arrow) within the posterior annulus at L4-5

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Transversely-tear or fissure of the annulus, running in the axial plane (horizontally), usually limited to rupture of the outer annular attachments to the ring apophysis. Transverse tears are usually small and are located at the junction of the annulus and ring apophysis. Concentrically-separation, or break, of annular fibers, in a plane roughly parallel to the curve of the periphery of the disc, creating fluid-filled spaces between adjacent annular lamellae.

protrusion and an asymmetrical disc bulge is often open to individual interpretation. This lack of consistency is also prevalent in the literature with a variety of definitions being used. By definition, herniation is displacement of disc material beyond the limits of the intervertebral disc space. Based on the type of displacement various nomenclatures are in use.31,32

Disc Herniation Nomenclature

Axial Plane Zones (Fig. 17.44)

Standardized disc pathology nomenclature and classification in magnetic resonance imaging were published in 2001 by the Combined Task Force of the North American Spine Society, American Society of Spine Radiology and the American Society of Neuroradiology and subsequently endorsed by other professional organizations and scientific societies.P Despite multiple articles published in recent years quoting standardized terminology recommendations from 2001 there is still a wide variety of radiological interpretation of what constitutes a particular disc pathology. For example, the distinction between a disc

The center of the central zone is a sagittal plane through the center of the vertebral body.

Fig. 17.44 Schematic representation of the anatomical zones identified on an axial T2-weighted image

Central zone

Subarticular (lateral recess) zone (Fig. 17.46)

The subarticular zone cannot be precisely delineated because the structures that define the planes of the zone are irregular. Forminal zone (Fig. 17.47)

Sometimes called the "pedicle zone," which can be confusing because pedicle zone might also refer to measurements in the sagittal plane between the upper and lower surfaces of a given pedicle, which is properly called pedicle level.

Fig. 17.45 Axial T2-weighted lumbar spine MRI image showing L4/5 focal posterior central disc herniation-protrusion (arrow)

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Fig. 17.46 Axial T2-weighted lumbar spine MRI image showing right subarticular disc herniation (arrow)

Fig. 17.47 Axial T2-weighted lumbar spine MRI. Right foraminal disc herniation (arrows)

Extraforaminal zone: Also referred to as far

lateral zone. Craniocaudal (Sagittal) Plane Levels

• Disc level-confined to between the vertebral endplates • Suprapedicular level-between superior endplate and superior border of pedicle • Pedicle level-at the level of the pedicle • Infrapedicular level-below lower margin of the pedicle to the inferior endplate. Classification Based on Volume of Displaced Material

• Mild-medullary canal compromise less than one-third • Moderate-medullary canal compromise between one-third and two-thirds (Fig. 17 .48) • Severe-medullary canal compromise more than two-thirds. Disc herniations may be further specifically described as: • Contained (sub-annular herniation) when displaced disc tissue is wholly within an outer perimeter of uninterrupted outer annulus or capsule

Fig. 17.48 Axial T2-weighted lumbar spine MRI image showing L3/4 central focal disc protrusion with moderate canal stenosis (arrow)

• Uncontained when displaced disc material is not contained by outer annulus. Disc Herniation-Protrusion

• Described when the greatest plane in any direction between the edges of the protruded disc material beyond the disc is less than the distance between the edges of the base. • Focal-base less than 25% (90°) of disc circumference (Fig. 17.49).

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• May have a migrated fragment, if there is disc material which is displaced away from the site of the extrusion, and can be either above or below the disc space migration refers to the position of the displaced disc material, rather than to its continuity with disc tissue within the disc of origin, therefore, it is not synonymous with sequestration. • Can be further specified as a sequestration if the displaced disc material has completely lost continuity with the parent disc (Fig. 17.51). Intra vertebral Herniation (Fig. 17 .52)

Fig. 17.49 Axial T2-weighted lumbar spine MRI image showing L2/3 central focal disc protrusion with central annular disc tear (arrow)

• Broad based-base 25-50% (90-180°) of disc

circumference. Disc Herniation-Extrusion (Fig. 17 .50)

• Described when at least one plane of any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base measured in the same plane.

A disc in which a portion of the disc is displaced through the endplate into the centrum of the vertebral body. Spinal Stenosis

Spinal MRI is most useful in delineating the location and extent of stenosis. Both modalities will clearly show the severity of the disease and delineate the anterior and posterior structures that are the cause of the stenosis. In the cervical region the canal is frequently encroached upon by posteriorly directed ridges, calcified herniated discs, and hypertrophic, and at times, ossified posterior longitudinal ligament. From the back the canal

Figs 17.50A and B L5/S1 disc extrusion-L5/S1 disc extrusion compressing the right S1 nerve root

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Fig. 17.51 Sequestrated disc L4-5 migrated cranially

Fig. 17.52 Herniation through endplates into vertebral body. Note, edema around herniation

may be encroached upon by hypertrophic facets and thickened ligamenta £lava (Fig. 17.53).

In the lumbar spine hypertrophic facets and thickened ligamenta flava are the most common offending structures. Not infrequently facet cysts play a role in symptom production (Fig. 17.54). The spinal canal may be further compromised by degenerative unstable segments. In the cervical region, facet hypertrophy in combination with uncovertebral joint hypertrophy compromise the neural foramina and lead to nerve root dysfunction. MRI of the cervical spine, in sagittal and axial cuts, will provide invaluable information about the spinal cord. Quite frequently an increased cord signal is seen on T2-weighted images of the compressed segments. Spine Infections

Fig. 17.53 Sagittal T2-weighted MRI depicting disc herniations at C3-4 and C4-5 intervertebral spaces compressing the cord posteriorly toward the hypertrophied ligamenta flava. There is severe cord compression at C3-4 (arrow). The cord signal is increased due to myelomalacia or gliosis

MRI, the diagnostic modality of choice, is highly sensitive and specific and may confirm the presence of infection at an early stage of the disease. Tl-weighted images will show decreased signal in the involved vertebral bodies, especially at the end plate region. As a result, the disc and the bone signal may appear similar in intensity. The endplate margins may

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215

Figs 17.54A and B Axial (A) and sagittal (B). T2-weighted MRI of the lumbar spine showing a facet joint synovial cyst (arrow) bulging into the spinal canal. Note that the facet signal is similar to that of the CSF and it does not enhance with gadolinium

look fuzzy, and interruption of cortical continuity may be seen. T2-weighted images will show increased signal of both the disc and the affected vertebral body (Fig. 17.55). Inlate stages of osteomyelitis, when bone sclerosis occurs, T2-weighted images will show decreased signal due to the obliteration of the bone marrow and increased production of bone. The presence of gas within the vertebral body will result in decreased signal on Tl- as well as T2-weighted images. Following contrast administration, the

affected discs and bones will show clear enhancement even at the early stages of the disease.33 Pott's Spine

On MRI the affected vertebral bodies will appear hypointense on Tl -weighted images and hyperintense on T2-weighted images, especially in the subchondral region. No enhancement of the discs is seen in the early stages of the disease. This helps differentiate TB spondylitis from pyogenic spondylitis. Paraspinal abscesses appear hypointense on TlWI and hyperintense on T2WI (Fig. 17.56). Diffuse enhancement may appear on Tl WI following contrast administration. Axial cuts are very important in assessing spinal cord integrity (Fig. 17.57). QUANTITATIVE SENSORY TESTING Description

Fig. 17.55 Sagittal T1WI with contrast shows enhancement in the vertebral bodies and the intervening disc. Most of the disc has been destroyed

Quantitative sensory testing (QST) systems have been investigated for the noninvasive assessment and quantification of sensory nerve function in individuals with symptoms of, or the potential for, neurologic damage or disease. Pain conditions evaluated may include diabetic neuropathy and uremic and toxic neuropathies, complex regional pain syndrome, carpal tunnel syndrome, and other nerve entrapment/ compression disorders or damage.

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Fig. 17 .56 Sagittal T2-weighted MR image showing destruction of three thoracic vertebrae with abscess formation and spinal cord compression. Note the increased signal within the vertebral body above the abscess

Fig. 17.57 Sagittal T1WI with contrast discloses the full extent of the infectious process: There is marked enhancement of the infiltrated, thick epidural fat anterior and posterior to the dural sac

QST systems measure and quantify the amount of physical stimuli required for sensory perception to occur in the individual. As sensory deficits increase, the perception threshold of QST will increase, which may be informative in documenting progression of neurologic damage or disease. QST has not been established for use as a sole tool for diagnosis and management, but has been investigated in conjunction with standard evaluation and management procedures (e.g. physical and neurological examination, monofilament testing, pinprick, grip and pinch strength, Tinel, Phalen and Roos sign) to attempt to enhance the diagnosis and treatment planning process and confirm physical findings with quantifiable data. Stimuli used in QST includes touch, pressure, pain, thermal (warm and cold), or vibratory stimuli. The gold standard for evaluation of myelinated large fibers is the electromyographic nerve conduction study (EMGNCS). However, the function of smaller myelinated and unmyelinated sensory nerves,

which may show pathologic changes before the involvement of the motor nerves, cannot be detected by nerve conduction studies. FUNCTIONAL MRI AND CHRONIC PAIN

Recent advances in functional imaging have revolutionized our concept of central process of pain. Indeed, it seems that we are on the verge of using this technology to reach a fundamental new understanding of clinical pain, particularly chronic pain. Functional imaging has already redefined chronic pain as a degenerative disease, and has shed some light on complex diseases such as fibromyalgia. Since brain responses are the final common pathway in behavioral responses to pain (unconscious and conscious), it is believed that the application of functional imaging will allow us to categorize pain conditions in an objective manner and to better understand the underlying circuitry and identify targets for a new generation of analgesics.

Common Investigations in Pain Medicine

Functional MRI measures neural activity by an indirect evaluation of changes in blood flow in capillary beds. Functional MRI (fMRI) is based on the increase in blood flow to the local vasculature that accompanies neural activity in the brain. This results in a corresponding local reduction in deoxyhemoglobin because the increase in blood flow occurs without an increase of similar magnitude in oxygen extraction. Since deoxyhemoglobin is paramagnetic, it alters the T2-weighted magnetic resonance image signal. Thus, deoxyhemoglobin is sometimes referred to as an endogenous contrast enhancing agent, and serves as the source of the signal for fMRI. A new technology, functional magnetic resonance imaging (fMRI), which allows researchers to view brain activity in near-real time, is opening a window into the brain. Functional MRI has revealed that chronic pain is largely processed in a different brain region than acute pain, which explains why treatments for acute pain have a little effect on chronic pain. The technology has opened the door to biofeedback pain control as well as improved testing of new drugs and other therapies.

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