Minimally Invasive Percutaneous Spinal Techniques E-Book
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Minimally Invasive Percutaneous Spinal Techniques E-Book

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Minimally Invasive Percutaneous Spinal Techniques, by Daniel H. Kim, MD, FACS, Kyung Hoon Kim, MD, and Yong Chul Kim, MD, helps you apply methods of spinal pain relief that involve less risk and shorter recovery times. Focusing on the broad appeal of this goal for you and your patients, this volume will help surgeons and specialists in various areas of pain management provide less invasive alternatives and faster recovery procedures for those suffering with spinal injuries. Step-by-step techniques are well-illustrated in the book and demonstrated extensively online.

  • Get accurate, step-by-step guidance by reviewing full-color, richly illustrated descriptions of various techniques.
  • Make the most of extensive surgical videos demonstrating many of the procedures from the book on expertconsult.com.
  • Reduce the risk associated with invasive spinal procedures by considering new perspectives on pain management techniques that can be used by specialists from various disciplines.
  • Address the growing need for less invasive surgeries with shorter recovery times among a large and aging population with musculoskeletal problems.

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Date de parution 28 septembre 2010
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EAN13 9780702043338
Langue English
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Minimally Invasive Percutaneous Spinal Techniques

Daniel H. Kim, MD, FACS
Professor, Baylor College of Medicine, Department of Neurosurgery, Houston, Texas

Yong-Chul Kim, MD, PhD
Professor, Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine
Director, Pain Management Center, Seoul National University Hospital, Seoul, Korea

Kyung-Hoon Kim, MD, PhD
Associate Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Pusan, Korea
Saunders
Front matter

Minimally invasive percutaneous spinal techniques
Daniel H. Kim, MD, FACS , Professor, Baylor College of Medicine, Department of Neurosurgery, Houston, Texas
Yong-Chul Kim, MD, PhD , Professor, Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Director, Pain Management Center, Seoul National University Hospital, Seoul, Korea
Kyung-Hoon Kim, MD, PhD , Associate Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Pusan, Korea
Copyright

1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
MINIMALLY INVASIVE PERCUTANEOUS SPINAL TECHNIQUES
ISBN: 978-0-7020-2913-4
Copyright © 2011 by Saunders, an imprint of Elsevier Inc.
All rights reserved. No part of this publication 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 publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions .
This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).

Notice
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the [Editors/Authors] assumes any liability for any injury and/or damage to persons or property arising out of or related to any use of the material contained in this book.
The Publisher
Library of Congress Cataloging-in-Publication Data
Minimally invasive percutaneous spinal techniques / [edited by] Daniel H. Kim. – 1st ed.
p.; cm.
Includes bibliographical references and index.
ISBN 978-0-7020-2913-4
1. Spine–Endoscopic surgery. 2. Injections, Spinal. I. Kim, Daniel H.
[DNLM: 1. Spinal Cord–surgery. 2. Nerve Block. 3. Spine–surgery. 4. Surgical Procedures, Minimally Invasive–methods. WL 400 M665 2010]
RD768.M537 2010
617.5’60597–dc22
2010007303
Acquisitions Editor: Daniel Pepper
Developmental Editor: Janice Gaillard
Publishing Services Manager: Rajendrababu Hemamalini
Project Manager: Srikumar Narayanan
Design Direction: Steve Stave
Printed in Canada
Last digit is the print number: 9 8 7 6 5 4 3 2 1
Dedication
To my loving parents, Kim Chan Taek and Kim Shin Ja.
Daniel H. Kim
To my wonderful wife, Eun-Sook Choi, my son and daughter, Yeong-Joong Kim and Min-Seung Kim, and my mother Sam-Soon Lee.
Yong-Chul Kim
This book is dedicated to my family, Clinic, Department, Pusan National University, and Korea.
Kyung-Hoon Kim
List of Contributors

Yong Ahn, MD, PhD, Vice President, Wooridul Spine Hospital, Seoul, Korea

Carlos F. Arias, MD, Department of Minimally Invasive Reconstructive and Arthroplasty Spine Surgery, Santa Rita Hospital, Sao Paulo, Brazil

Seung-Hun Baek, MD, PhD, Assistant Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Seong-Wan Baik, MD, PhD, Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Sung-Bae Ban, MD, Director, Department of Neurosurgery, Daegu Wooridul Spine Hospital, Wooridul Spine Hospital, Daegu, Korea

Walter Bini, MD, FRCS, Department of Neurosurgery, Post Graduate Studies, University of Hannover Medical School (MHH), Hannover, Germany

John Chiu, MD, Chairman and Director, Neurospine Division, Department of Neurosurgery, California Spine Institute, Thousand Oaks, California

Sang-Sik Choi, MD, Associate Professor, Department of Anesthesiology and Pain Medicine, Korea University College of Medicine, Seoul, Korea

Won-Chul Choi, MD, President, Daegu Wooridul Spine Hospital, Wooridul Spine Hospital, Daegu, Korea

Won-Gyu Choi, MD, PhD, President, Busan Wooridul Spine Hospital, Dongrae-gu, Busan, Korea

Etevaldo Coutinho, MD, Department of Minimally Invasive, Reconstructive and Arthroplasty Spine Surgery, Santa Rita Hospital, Sao Paulo, Brazil

Fabio P. Furieri, MD, Advanced Orthopaedics of South Florida, Lake Worth, Florida

Jee-Soo Jang, MD, PhD, President, Seoul Wooridul Hospital, Seoul, Korea

Ho-Yeong Kang, MD, President, Dongrae Wooridul Spine Hospital, Department of Radiology, Busan, Korea

Cheul-Hong Kim, MD, PhD, Associate Professor, Department of Anesthesia and Pain Medicine School of Dentistry, Pusan National University, Busan, Korea

Daniel H. Kim, MD, FACS, Professor, Baylor College of Medicine, Department of Neurosurgery, Houston, Texas

Hae-Kyu Kim, MD, PhD, Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Hak-Jin Kim, MD, PhD, Professor, Department of Radiology, School of Medicine, Pusan National University, Busan, Korea

Inn-Se Kim, MD, PhD, Professor and President, Pusan National University, Busan, Korea

Kyung-Hoon Kim, MD, PhD, Associate Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Seong Oh Kim, MD, Zelkova Pain Clinic, Seoul, Korea

Tae-Kyun Kim, MD, PhD, Assistant Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Yong-Chul Kim, MD, PhD, Professor, Department of Anesthesiology and Pain Medicine, Seoul National University College of Medicine, Director, Pain Management Center, Seoul National University Hospital, Seoul, Korea

Jae-Young Kwon, MD, PhD, Chairman and Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Chul-Joong Lee, MD, PhD, Assistant Professor, Department of Anesthesiology and Pain Medicine, Sungkyun, kwan University School of Medicine, Samsung Seoul Hospital, Samsung Medical Center, Seoul, Korea

Ho-Yeon Lee, MD, PhD, President, Seoul Chungdam Wooridul Spine Hospital, Seoul, Korea

Hyeon-Jung Lee, MD, PhD, Assistant Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

In-Sook Lee, MD, Assistant Professor, Department of Radiology, School of Medicine, Pusan National University, Busan, Korea

Mi-Guem Lee, MD, Clinical Instructor, Department of Anesthesiology and Pain Medicine, Korea University Guro Hospital, Seoul, Korea

Mi-Kyung Lee, MD, PhD, Professor, Department of Anesthesiology and Pain Medicine, Korea University College of Medicine, Chairman, Korea University Guro Hospital, Seoul, Korea

Pyung-Bok Lee, MD, PhD, Assistant Professor, Pain Medicine Specialist, Department of Anesthesiology and Pain Medicine, Seoul National University Bundang Hospital, Seong-nam, Korea

Sang-Chul Lee, MD, PhD, Professor, Department of Anesthesiology and Pain, Medicine, Seoul National University College of Medicine, Chairman, Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul, Korea

Sang-Ho Lee, MD, PhD, Chairman, Wooridul Hospital, Seoul, Korea

Seung-Cheol Lee, MD, Wooridul Hospital, Seoul, Korea

Hansjorg Franz Leu, MD, Bethania Spine Base, Zurich, Switzerland

Juliano Lhamby, MD, Santa Rita Hospital, Spine Surgery Service, Sao Paulo, Brazil

Jason S. Mazza, MSc, OPA-C, Palm Harbor, Florida

Leonardo Oliveira, BSc, Department of Minimally Invasive Reconstructive and Arthroplasty Spine Surgery Santa Rita Hospital, Sao Paulo, Brazil

Luiz M. Pimenta, MD, PhD, Department of Minimally Invasive, Reconstructive and Arthroplasty Spine Surgery, Santa Rita Hospital, Sao Paulo, Brazil

Merrill W. Reuter, MD, PhD, Chairman, Department of Orthopaedic Surgery, Advanced Orthopaedics of South Florida, Lake Worth, Florida

Sebastian Ruetten, MD, PhD, Head, Department of Spine Surgery and Pain Therapy, Center for Orthopaedics and Traumatology, St. Anna-Hospital Herne, University of Witten/Herdecke, Herne, Germany

Thomas Schaffa, MD, Department of Minimally Invasive, Reconstructive and Arthroplasty Spine Surgery, Santa Rita Hospital, Sao Paulo, Brazil

Chan-Shik Shim, MD, PhD, Vice President, Seoul Chungdam Wooridul Spine Hospital, Seoul, Korea

John H. Shim, MD, MBA, FACS, Palm Harbor, Florida

Seung-Eun Shim, MD, PhD, Clinical Assistant Professor, Department of Anesthesiology and Pain Medicine, Director, Pain Management Center, SMG-SNU Boramae Medical Center, Seoul, Korea

Sang-Wook Shin, MD, PhD, Associate Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea

Ji-Young Yoon, MD, Assistant Professor, Department of Anesthesia and Pain Medicine, School of Medicine, Pusan National University, Busan, Korea
Preface

Daniel H. Kim

Yong-Chul Kim

Kyung-Hoon Kim
Advances in the safety and efficacy of spinal surgical techniques in the past decade have been nothing short of remarkable. As internationally recognized experts on many of these techniques, the authors of this book are uniquely qualified to share their expertise with other surgeons, surgical nurses, researchers, students, and members of industry who are interested in today’s innovative spinal procedures.
All clinicians involved in spinal surgery can benefit from this book as they work to improve diagnoses, techniques, and patient outcomes. The techniques described here are minimally invasive and are conducted percutaneously, which typically yields briefer surgeries, reduced patient hospital stays and recovery times, and improved patient outcomes—results that are a boon to clinicians and patients alike.
This book begins with a review of spinal anatomy and pathologies before delving into an extensive discussion of current approaches to palliative procedures and the latest in minimally invasive percutaneous surgical techniques. Each chapter provides detailed descriptions of the components of a successful procedure, including the advantages, disadvantages, indications, and contraindications for each technique. In the final chapter, the book culminates in a discussion of outcome measurements for the techniques described.
The easy to follow format is organized with headings and bullets that allow readers to quickly grasp essential information. Hundreds of detailed, high-quality illustrations, intraoperative photographs, and radiographic images enhance the text further, helping to clarify the information presented on each topic.
Understanding the techniques in this book is important for a thorough knowledge of the spinal surgery field today; the best course of treatment for a patient may be one described here. This book covers more than a dozen palliative techniques and over twenty minimally invasive procedures, including those incorporating new technologies, innovative techniques such as endoscopic cervical microdecompression of the disc and foramen, and posterolateral approaches to surgeries like thoracic discectomy and lumbar nuclectomy.
Every medical professional faces the dual constraints of limited time and almost unlimited new information. It is essential to have a resource that provides sufficient detail and instruction on new procedures while still being concise. Minimally Invasive Percutaneous Spinal Techniques consolidates pertinent information about the latest techniques into a single source, creating an invaluable clinical resource.

Acknowledgments
I would like to thank Sarah Campbell and Lara Richards for their tireless work, as well as all the others who have contributed their energy, expertise, and talents to make this book what it is.
I would like to acknowledge my colleagues, residents, nurses, and technicians for their help on this book.
I thank my family, Sung-Suk Seo, Na-Ryun Kim, Jung-Ryun Kim, Yong-Do Kim, and Bong-Young Lee, for their endless dedication and love.
Table of Contents
Instructions for online access
Front matter
Copyright
Dedication
List of Contributors
Preface
Chapter 1: Diagnosis and Treatment of Spinal Pain
Chapter 2: Current Understanding of Spinal Pain and the Nomenclature of Lumbar Disc Pathology
Chapter 3: Radiologic Anatomy of the Spine
Chapter 4: Imaging Diagnosis of the Degenerative Spine
Chapter 5: Epidural Blocks
Chapter 6: Transforaminal Epidural Block and Selective Nerve Root Block
Chapter 7: Dorsal Root Ganglion Pulsed Radiofrequency Lesioning
Chapter 8: Medial Branch Block and Radiofrequency Lesioning
Chapter 9: Atlantooccipital and Atlantoaxial Joint Block for Cervicogenic Headache
Chapter 10: Sympathetic Nerve Block and Neurolysis
Chapter 11: Sacroiliac Joint Block and Neuroablation
Chapter 12: Paravertebral Block
Chapter 13: Intervertebral Discography
Chapter 14: Epiduroscopic Adhesiolysis
Chapter 15: Spinal Cord Stimulation
Chapter 16: Implantation of Intrathecal Drug Delivery Systems
Chapter 17: Intradiscal Therapies
Chapter 18: Kyphoplasty
Chapter 19: Unipedicular Approach for Percutaneous Vertebroplasty
Chapter 20: Percutaneous Sacroplasty
Chapter 21: Anterior Endoscopic Cervical Discectomy
Chapter 22: Anterior Endoscopic Cervical Microdecompression of Disc and Foramen
Chapter 23: Percutaneous Endoscopic Cervical Discectomy and Stabilization
Chapter 24: Endoscopy-Assisted Thoracic Microdiscectomy
Chapter 25: Posterolateral Endoscopic Thoracic Discectomy
Chapter 26: Selective Percutaneous Posterolateral Endoscopic Lumbar Nuclectomy
Chapter 27: Full-Endoscopic Interlaminar Lumbar Discectomy and Spinal Decompression
Chapter 28: Posterior Lumbar Foraminal Decompression
Chapter 29: Percutaneous Transforaminal Lumbar Interbody Stabilization
Chapter 30: Percutaneous Pedicle Screw Fixation
Chapter 31: Percutaneous Translaminar Facet Pedicle Screw Fixation
Chapter 32: Percutaneous Lumbar Restabilization via a Posterolateral Approach
Chapter 33: Interspinous Spacers
Chapter 34: Lateral Percutaneous Interspinous System for the Treatment of Lumbar Stenosis
Chapter 35: Minimally Invasive Percutaneous Lumbar Fusion Technique
Chapter 36: Transaxial Anterior Lumbar Interbody Fusion Using the AxiaLIF System
Chapter 37: Lateral Interbody Fusion Using the XLIF System
Chapter 38: Outcome Measurements for Minimally Invasive Percutaneous Spine Techniques
Index
Chapter 1 Diagnosis and Treatment of Spinal Pain

Kyung-Hoon Kim, MD, PhD, Daniel H. Kim, MD, FACS

Classifications of spinal pain
Low back pain (LBP) is defined as pain and discomfort that are localized below the costal margin and above the inferior gluteal folds with or without leg pain. LBP is further defined according to the duration of an episode: acute, less than 6 weeks; subacute , between 6 and 12 weeks; chronic , 12 weeks or more ( Table 1.1 ).
Table 1.1 Classification of Low Back Pain According to Duration of Episode Duration (Weeks) Classification and Comments <6
Acute
Self-limiting (recovery rate 90% within 6 weeks) 6-12 Subacute >12
Chronic
Develops in 2%-7% of people
Recurrent low back pain is defined as a new episode of pain that occurs after a symptom-free period of 6 months and is not an exacerbation of chronic LBP. A recurrent acute episode is an episode in which the current symptoms have persisted 6 weeks or less and had improved prior to the current episode, separating it from previous episodes.
Nonspecific low back pain is defined as low back pain that is not attributed to recognizable, known, specific pathology (e.g., infection, tumor, osteoporosis, ankylosing spondylitis, fracture, inflammatory process, radicular syndrome, or cauda equina syndrome) ( Box 1.1 ).

BOX 1.1 Three Categories (Or Diagnostic Triage) of Acute Low Back Pain

Serious spinal pathology: “Red flag” conditions, such as tumor, infection, inflammatory disorder, fracture, and cauda equina syndrome
Nerve root pain/radicular pain: Numbness and weakness in the legs and presence of sciatica
Nonspecific low back pain: Low back pain not attributed to recognizable, known, specific pathology
Chronic pain is defined as pain that:
▪ Persists a month beyond the usual course of an acute disease or beyond a reasonable time for any injury to heal and is associated with chronic pathologic processes that cause continuous pain or pain at intervals for months or years.
▪ Persists and does not respond to routine pain control methods .
▪ Exists beyond an expected time frame for healing .
▪ Is caused by an injury or condition that may never heal.
The four diagnostic categories of LBP according to ICD-9 ( International Classification of Diseases and Related Health Problems, 9th revision) [1] in the absence of symptoms that suggest serious underlying disease (e.g., cancer, cauda equina syndrome, significant or progressive neurologic deficit, or other systemic illness) are as follows:
Acute LBP: LBP that does not radiate past the knee and with current symptoms 6 weeks or less from onset ( Table 1.2 ).
Chronic LBP: LBP that does not radiate past the knee and with current symptoms more than 6 weeks from onset.
Acute sciatica: LBP that radiates past the knee and with current symptoms 6 weeks or less from onset.
Chronic sciatica: LBP that radiates past the knee and with current symptoms more than 6 weeks from onset.
Table 1.2 Diagnosis and Treatment of Acute Low Back Pain Diagnosis Treatment Recommended Not Recommended D1: Undertake diagnostic triage (serious spinal pathology, nerve root pain/radicular pain, or nonspecific low back pain), consisting of appropriate history and physical examination, at the first assessment. T1: Give adequate information and reassure the patient. T2: Prescription of bed rest as a treatment. D2: Assess for psychosocial risk factors (yellow flags; see Table 1.3 ) and review them in detail if there is no improvement. T3: Advise the patient to stay active and to continue normal daily activities, including work if possible. T4: Specific exercises for acute low back pain. D3: Diagnostic imaging tests (including radiographs, CT, and MRI) are not routinely indicated for acute low back pain. T5: Prescribe medication, if necessary, for pain relief. T6: Epidural corticosteroid injections for acute nonspecific low back pain. D4: Reassess the patient whose symptoms fail to resolve. T7: Consider spinal manipulation for patients who are failing to return to normal activities.T13: Consider multidisciplinary treatment programs in occupational settings for workers on sick leave for more than 4-8 weeks. T8: “Back schools” for treatment of acute low back pain.T9: Behavioral therapy for treatment of acute low back pain.T10: Traction.T11: Massage as a treatment for acute nonspecific low back pain.T12: Transcutaneous electrical nerve stimulation (TENS) as a treatment for acute nonspecific low back pain.
Diagnostic triage of acute LBP consists of the following conditions (see Box 1.1 ):
▪ Serious spinal pathology
▪ Nerve root pain/radicular pain
▪ Nonspecific LBP
Red flags in the diagnosis of LBP are signs that a serious spinal pathology may be the cause of the LBP; they are listed in Table 1.3 :
Table 1.3 Red and Yellow Flags in Diagnosis of Low Back Pain Red flags (signs of serious pathology)
Patient’s age at onset < 20 years or > 55 years
Recent history of violent trauma
Constant progressive, nonmechanical pain (no relief with bed rest)
Thoracic pain
Past medical history of malignant tumor
Prolonged use of corticosteroids
Drug abuse, immunosuppression, human immunodeficiency virus
Systemic “unwellness”
Unexplained weight loss
Widespread neurologic symptoms (including cauda equina syndrome)
Structural deformity
Fever Yellow flags (psychosocial risk factors)
Inappropriate attitudes and benefits about back pain (e.g., belief that back pain is potentially harmful or severely disabling, high expectations of passive treatments rather than belief that active participation will help)
Inappropriate pain behavior (e.g., fear-avoidance behavior and reduced activity levels)
Work-related problems or compensatory issues (e.g., poor work satisfaction)
Emotional problems (e.g., depression, anxiety, stress, tendency to low mood, withdrawal from social interaction)
Signs or symptoms of neurologic involvement in a patient with LBP are complaint of numbness or weakness in the legs and sciatica with radiation past the knee. The following features apply to possible diagnosis of sciatica:
▪ When pain radiates only to the posterior thigh, it is less likely that the pain is caused by a true radiculopathy.
▪ Sciatica has such a high sensitivity (95%) that its absence makes lumbar disc herniation unlikely.
▪ The likelihood of disc herniation in a patient without sciatica would be 1 in 1000.
Because more than 95% of lumbar disc herniations occur at the L4-L5 or L5-S1 level, the neurologic examination should focus on the L5 and S1 nerve roots; however, upper lumbar nerve root involvement may be suggested when pain conforms to an L2, L3, or L4 dermatomal distribution and is accompanied by anatomically congruent motor weakness or reflex changes.
Psychosocial yellow flags are patient factors that increase the risk for development or perpetuation of chronic pain and long-term disability (including work loss associated with LBP); examples are listed in Table 1.3 . Identification of yellow flags should lead to appropriate cognitive and behavioral management.

Considerations for diagnosis
Cauda equina syndrome is a condition requiring emergency evaluation and surgery. A patient with LBP should be referred immediately to the emergency room if any of the following emergency symptoms is present:
▪ Sudden onset of or otherwise unexplained loss of or changes in bowel or bladder control (retention or incontinence)
▪ Sudden onset of or otherwise unexplained bilateral leg weakness
▪ Saddle numbness
A patient should be examined within 24 hours if the patient requests a same-day appointment or any of the following urgent symptoms is present:
▪ Fever (38° C or 100.4° F) for more than 48 hours
▪ Unrelenting night pain or pain at rest
▪ Pain with distal (below the knee) numbness or weakness of leg(s)
▪ Progressive neurologic deficit
Is evaluation indicated? A patient should be offered an appointment within 2 to 7 days if any of the following symptoms or patient factors is present:
▪ Exertion injury (e.g., lifting, digging, reaching)
▪ History of back symptoms—patient has been seen before, at least once
▪ Chronic back pain lasting longer than 6 weeks
▪ Unexplained weight loss (more than 10 pounds in 6 months)
▪ Age more than 50 years
▪ History of cancer
Performance of lumbar spine radiographs should be limited to presence of any of the following red flag indications:
▪ Unrelenting night pain or pain at rest
▪ Fever above 38° C or 100.4° F for more than 48 hours
▪ Progressive neuromotor deficit
▪ Pain with distal numbness or leg weakness
▪ Loss of bowel or bladder control (retention or incontinence)
▪ Clinical suspicion of ankylosing spondylitis
▪ Significant trauma
▪ History or suspicion of cancer
▪ Osteoporosis
▪ Long-term oral steroid therapy
▪ Immunosuppression or immunosuppressive therapy
▪ Drug or alcohol abuse
Advanced imaging studies should be performed only for the patient with the following findings:
▪ Progressive neurologic deficit
▪ Minimal to no improvement of radicular symptoms despite 6 weeks of conservative treatment
▪ Uncontrolled pain
▪ Cauda equina syndrome

Epidemiology of low back pain
The lifetime prevalence of LBP is reported as more than 70% in industrialized countries (1-year prevalence, 15% to 45%; adult incidence, 5% per year). Peak prevalence occurs between ages 35 and 55.
Symptoms, pathology, and radiologic appearances in patients with LBP are poorly correlated. Pain is not attributable to pathology or neurologic encroachment in about 85% of people. About 4% of people seen with LBP in primary care have compression fractures, and about 1% have a neoplasm. Ankylosing spondylitis and spinal infections are even more rare. The prevalence of prolapsed intervertebral disc is about 1% to 3%.
Risk factors for LBP are poorly understood. The most frequently reported are as follows:
1. Heavy physical work.
2. Frequent bending, twisting, lifting, pulling and pushing.
3. Repetitive work.
4. Static postures.
5. Vibrations.
6. Psychosocial risk factors, including stress, distress, anxiety, depression, cognitive dysfunction, pain behavior, job dissatisfaction, and mental stress at work.

Outcomes
The aims of treatment for acute LBP are as follows:
▪ To relieve pain
▪ To improve functional ability
▪ To prevent recurrence and chronicity
Relevant outcomes for acute LBP are as follows:
▪ Overall improvement in pain intensity
▪ Improvement in back pain–specific functional status
▪ Positive impact on employment
▪ Improvement in generic functional status
▪ Decrease in medication use
Intervention-specific outcomes may also be relevant; examples are as follows:
▪ Behavioral treatment may improve coping and pain behavior.
▪ Exercise therapy may improve strength and flexibility.
▪ Antidepressants may decrease the symptoms of depression.
▪ Muscle relaxants may reduce the symptoms of muscle spasm.

Treatment of Acute Low Back Pain in Primary Care
The aims of treatment for acute LBP in primary care are to:
▪ Provide adequate information, reassuring the patient that LBP is usually not a serious disease and that rapid recovery is expected in most cases.
▪ Provide adequate symptom control, if necessary.
▪ Encourage the patient to stay as active as possible and to return to normal activities, including work, as early as possible.
▪ Emphasize patient education and conservative home self-care.
An active approach is the best treatment option for acute LBP. Passive treatment modalities (for example, bed rest, massage, ultrasound, electrotherapy, laser, and traction) should be avoided as monotherapy and should not be routinely be used, because they may increase the risk of illness behavior and chronicity.
Patient education and conservative home self-care consist of the following activities and medications:
▪ Limited bed rest
▪ Early ambulation
▪ Postural advice
▪ Gentle stretching
▪ Use of ice/heat
▪ Anti-inflammatory and analgesic over-the-counter medications
▪ Early return to work or activities
Patients with acute LBP should be advised to stay active and continue ordinary and daily activity within the limits permitted by the pain . For chronic back pain, there is evidence that exercise therapy is effective.
Acute LBP is usually self-limiting (the recovery rate is 90% within 6 weeks), but chronic pain develops in 2% to 7% of people. Recurrent LBP and chronic LBP account for 75% to 85% of total worker absenteeism.

Natural History of Low Back Pain
Acute LBP is usually self-limiting (the recovery rate is 90% within 6 weeks), but chronic pain develops in 2% to 7% of people. Recurrent LBP and chronic LBP account for 75% to 85% of total worker absenteeism. Most patients will experience partial improvement in 4 to 6 weeks and have a recurrence of LBP in 12 months .

A General Assessment of Patients Reporting Low Back Pain
The patient presenting for low back pain should undergo assessment that establishes answers to the following questions:
▪ Has the patient had any recent back procedure or epidural anesthesia?
▪ What is the location of pain—simple LBP (does not radiate past the knee) versus sciatica (LBP with radiation past the knee)?
▪ What is the duration of symptoms, including date of injury or onset of symptoms? LBP for 6 weeks or less is acute; LBP for more than 6 weeks is chronic.
▪ If the pain is a result of an injury, how did the injury occur?
▪ Is the patient experiencing unrelenting or severe pain—rated on a scale of 0 to 10, with 10 indicating most severe pain?
▪ Are other medical conditions present?
▪ Does the patient have a history of previous back pain or surgery?
▪ Are any psychosocial factors present?
Psychosocial Factors to consider include the following:
▪ Belief that pain and activity are harmful
▪ “Sickness behavior” such as extended rest
▪ Depressed or negative moods, social withdrawal
▪ Self-treatment that does not fit best practice
▪ Problems with disability claim and compensation
▪ History of back pain, time off, or other claim
▪ Problems at work or low job satisfaction
▪ Heavy work, unsociable hours
▪ Overprotective family or lack of support
▪ Other factors, such as fear, financial problems, anger, depression, job dissatisfaction, family problems, and stress, that can contribute to prolonged disability

Relevant Medical History
Key elements of the patient’s medical history when symptoms of spinal pain are present ( Boxes 1.2 to 1.4 and Table 1.4 ) are as follows:
▪ Chief complaint
▪ History of present illness: location, character, severity, duration and timing, context, modifying factors, and associated signs and symptoms
▪ Review of systems
▪ Past history of interventional pain management: history of past pain problems, motor vehicle accidents, and occupational or nonoccupational injuries
▪ Family history: history of pain problems in the family, degenerative disorders, familial disorders, drug dependency, alcoholism, and drug abuse
▪ Psychological disorders: depression, anxiety, schizophrenia, and suicidal tendencies
▪ Social history: environmental information, education, marital status, children, habits, hobbies, and occupational history

BOX 1.2 Waddell Embellishment Tests That Indicate Nonorganic Pathology For Low Back Pain
Modified from Waddell G: 1987 Volvo award in clinical sciences: A new clinical model for the treatment of low-back pain. Spine 1987;12:632-644.

Tests

1. Tenderness : Subcutaneous (or less) pressure reproduces symptoms.
2. Stimulation of symptoms:
a. Loading the spine with the weight of the examiner’s hands on top of the patient’s head (to reproduce back symptoms).
b. Simulation of twisting the trunk when rotating the shoulders and hips in unison to reproduce back pain (can physiologically reproduce sciatica).
3. Distraction : Sitting knee extension to rest sciatic tension while distracting the patient with knee or foot examination as the reason for extending the knee. (If the patient is comfortable during sitting knee extension, the straight-leg raising test result should not be positive; a positive result of that test is of questionable significance.)
4. Nonanatomic distribution of pain : As seen on a pain drawing (total body or outside the body) or demonstrated on muscle testing (intermittent efforts).
5. Overreaction : Grimacing, complaints, or suffering displays are inappropriate for the situation or maneuver.

Scoring
A score of 0 to 2 (up to two positive responses) is normal. Three to five positive responses (score of 3 to 5) warn the clinician that nonphysical interference may render the history and physical findings somewhat confusing (identifying a need for a greater focus on objective measures). The more positive Waddell test responses, the greater the chance that nonphysical factors may alter the patient’s response to the physician’s care and potentially lower the clinical expectations for an excellent outcome from both surgical and nonsurgical treatments.

BOX 1.3 Referral Guidelines For Presurgical Psychological Screening

Check for

▪ Excessive pain behavior
▪ Symptoms inconsistent with identified pathology
▪ High levels of depression or anxiety
▪ Sleep disturbance: insomnia or hypersomnia
▪ Excessively high or low expectations of surgical outcome
▪ Marital distress or sexual difficulties
▪ Negative attitude toward work or employer
▪ Emotional lability or mood swings
▪ Inability to work or greatly decreased functional ability (< 3 months)
▪ Large or escalating doses of narcotics or anxiolytics
▪ Litigation or continuing disability benefits resulting from spine injury

Guidelines for Referral
Presence of no or 1 item: Referral not needed unless desired by patient.
Presence of 2-4 items: Referral should be considered.
Presence of 4 or more items: Referral should be strongly considered.

BOX 1.4 Preoperative Psychological Screening Risk Factors For Poor Surgical Outcome
MMPI, Minnesota Multiphasic Personality Inventory.

Risk Factors
Personality factors:
▪ Pain sensitivity (MMPI hypochondriasis and hysteria elevations)
▪ Anger (MMPI psychopathic deviate elevation)
▪ Depression (MMPI depression elevations)
▪ Anxiety and obsessions (MMPI psychasthenia elevations)
Poor coping strategies:
▪ Catastrophizing (Coping Strategies Questionnaire)
▪ Low self-efficacy or pain control (Copying Strategies Questionnaire)
Behavioral factors:
▪ Spousal reinforcement of pain (West Haven-Yale Multidimensional Pain Inventory)
▪ Litigation pending
▪ Workers’ compensation
▪ Blaming employer for injury
Historic factors:
▪ Abuse and abandonment
▪ Past psychological treatment
▪ Multiple previous medical problems
▪ Substance abuse

Preoperative Psychological Screening Prognosis
Good: 0-4 risk factors
Fair: 5-8 risk factors
Poor: 9-14 risk factors
Table 1.4 History Taking for Spinal Pain Question/Subject Answer Diagnostic Significance Age Young Disc injuries, spondylolisthesis Middle age Sprain/strain, herniated disc, degenerative disc disease Elderly Spinal stenosis, herniated disc, degenerative disc disease, arthritis Pain: Character Radiating (shooting) Radiculopathy (herniated disc, spondylosis) Diffuse, dull, nonradiating Cervical or lumbar strain (soft tissue injury) Location Unilateral vs. bilateral
Unilateral: herniated disc
Bilateral: systemic or metabolic disease, space-occupying lesion Neck Cervical spondylosis, neck sprain, muscle strain Arm (± radiation) Cervical spondylosis (± myelopathy), neck sprain, muscle strain Lower back Degenerative disc disease, back sprain, muscle strain Legs (± radiation) Herniated disc, spinal stenosis Occurrence Night pain Tumor With activity Usually mechanical etiology Alleviated by Arm elevation Herniated cervical disc Sitting down Spinal stenosis (stenosis relieved) Exacerbated by Back extension Spinal stenosis (e.g., going down stairs) Trauma Motor vehicle accident (seatbelt?) Cervical strain (whiplash), cervical fractures, ligamentous injury Activity Sports (stretching injury) “Burners/stingers” (especially in football) Neurologic symptoms Pain, numbness, tingling Radiculopathy, neuropathy Spasticity, clumsiness Myelopathy Bowel or bladder symptoms Cauda equina syndrome Systemic complaints Fever, weight loss Infection, tumor

Physical Examination
A physical examination for patients with symptoms of spinal pain would include palpation for spinal tenderness, neuromuscular testing, and the straight-leg raise (SLR) test. Table 1.5 summarizes the examination, techniques, and their clinical application in the patient with a complaint of low back pain.

Table 1.5 Physical Examination of the Spine
Neuromuscular testing should be performed to evaluate the following aspects:
▪ Motor: ankle and greater toe dorsiflexion strength
▪ Reflex: ankle and knee reflexes
▪ Sensory: pinprick sensation in the medial, dorsal, and lateral aspect of the foot
Significant or progressive neuromotor deficit requires surgical consultation.
The SLR test should be performed bilaterally to evaluate for nerve root impingement including, but not limited to, disc herniation. A positive SLR test result is defined as the presence of pain in the posterior leg that radiates below the knee when the patient is lying supine and the hip is flexed 60 degrees or less; it is suggestive of disc herniation. A negative SLR test result rules out surgically significant disc herniation in 95% of cases.

Related anatomy and physiology
The spinal muscles on the neck and back are described in Tables 1.6 through 1.9 . The spinal nerves are described in Tables 1.10 through 1.15 and shown in Figures 1-1 and 1-2 . The spinal blood supply is shown in Figures 1-3 and 1-4 and described in Table 1.16 . The intervertebral foraminal ligaments of the lumbar spine are shown in Figure 1-5 .

Table 1.6 Anterior Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.7 Posterior Neck Muscles (Suboccipital Triangle): Origins, Insertions, Actions, and Related Innervations

Table 1.8 Superficial (Extrinsic) Posterior Neck and Back Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.9 Deep (Intrinsic) Posterior Neck and Back Neck Muscles: Origins, Insertions, Actions, and Related Innervations

Table 1.10 Anterior and Posterior Branches of the Spinal Nerves

Table 1.11 Cervical Plexus (C1-C4 Ventral Rami) behind Internal Jugular Vein and Sternocleidomastoid (SCM) Muscles

Table 1.12 Brachial Plexus

Table 1.13 Lumbar Plexus

Table 1.14 Sacral Plexus and Coccygeal Nerves
Table 1.15 Spinal Nerve Branches and the Territories They Supply Spinal nerve branch Motor visceromotor territory Sensory territory Ventral ramus All somatic muscles except for the intrinsic back muscles Skin of the lateral and naterior trunk wall and of the upper and lower limbs Dorsal ramus Intrinsic back muscles Posterior skin of the head and neck, skin of the back and buttock Menigeal ramus - Spinal meniges, ligaments of the spinal column, capsules of the facet joints White ramus communicans Carries preganglionic fibers from the spinal nerve to the sympathetic trunk (‘White’ because the preganglionic fibers are myelinated) - Gray ramus communicans * Carrries postganglionic fibers from the sympahetic trunk back to the spinal nerve (‘Gray’ because the fibers are unmyelinated) -
* Strictly speaking, the gray ramus communicans is not a spinal nerve branch but a branch passing from the sympathetic trunk to the spinal nerve.

Figure 1–1 Anterior view of the nerves of the trunk wall.

Figure 1–2 Branches of the spinal nerves. Formed by the union of the dorsal (sensory) and ventral (motor) roots, the approximately 1 cm–long spinal nerve courses through the intervertebral foramen and divides into five branches after exiting the vertebral canal (see Table 1.15 ).

Figure 1–3 Composite schema of blood supply to the spinal cord and nerve roots showing two regions of the cord. Note the distribution between medullary arteries and true radicular arteries and that the medullary arteries usually run a course that is independent of the roots. 1, Dorsolateral longitudinal artery; 2, proximal radicular artery (of dorsal root); 3, dorsal medullary artery; 4, dorsal root of the thoracic spinal nerve; 5, distal radicular artery (of dorsal root); 6, sinuvertebral nerve; 7, dorsal ramus of spinal nerve; 8, segmental artery; 9, dorsal central artery; 10, dorsal root ganglion; 11, anterior laminar artery; 12, ventral ramus of spinal nerve; 13, rami communicantes; 14, ventral root of spinal nerve; 15, proximal radicular artery of ventral root; 16, periradicular theca of dura; 17, dorsal meningeal branch of vertebromedullary artery; 18, dura; 19, ventral meningeal plexus; 20, great ventral medullar artery (great “radicular” artery of Adamkiewicz); 21, anterior (ventral) spinal artery; 22, vasa corona of spinal cord; 23, spinal nerve; 24, ventral medullary artery of thoracic cord.

Figure 1–4 Schema showing the venous relations of a lumbar vertebra. The divisions of the network are the internal vertebral plexus, which surrounds the dura and is drained by veins in the intervertebral foramina; the basivertebral veins on the back of the vertebral bodies, which drain a network in the marrow spaces of the vertebrae; and the external vertebral plexus, which lies on the anterior and lateral sides of the vertebral bodies and on the vertebral arches. 1, Dorsal external vertebral plexus; 2, dorsal epidural plexus; 3, ascending lumbar veins; 4, basivertebral vein; 5, anterior ventral external vertebral plexus; 6, lumbar segmental vein; 7, muscular vein from posterior abdominal wall; 8, circumferential channels (sinuses) of epidural plexus; 9, ventral epidural plexus; 10, internal ventral and dorsal venous plexus; 11, lateral ventral external vertebral plexus.

Table 1.16 Spinal Arteris *

Figure 1–5 Intervertebral foraminal ligaments of the lumbar spine: A, corporo-transverse superior and corporo-transverse inferior; B, superior transforaminal ligament ; C, mid- transforaminal ligament; D, inferior transforaminal ligament; E, posterior transforaminal ligament. Enlarged image shows all ligaments in context.
(Modified from Park HK, Rudrappa S, Dujovny M, Diaz FG: Intervertebral foraminal ligaments of the lumbar spine: Anatomy and biomechanics. Childs Nerv Syst 2001;17:275-282.)

Imaging studies
The indications for and advantages of magnetic resonance imaging (MRI) and computed tomography (CT) in the evaluation of low back pain are summarized in Table 1.17 .
Table 1.17 Magnetic Resonance Imaging (MRI) and Computed Tomography (CT): Indications and Advantages in the Evaluation of Low Back Pain   MRI CT Indications     Major or progressive neurologic deficit (e.g., foot drop or functionally limiting weakness such as hip flexion or knee extension) Yes Yes Cauda equina syndrome (loss of bowel or bladder control or saddle anesthesia) Yes Yes Progressively severe pain and debility despite conservative therapy Yes Yes Severe or incapacitating back or leg pain (e.g., requiring hospitalization, precluding walking, or significantly limiting the activities of daily living) Yes Yes Clinical or radiologic suspicion of neoplasm (e.g., lytic or sclerotic lesion on plain radiographs, history of cancer, unexplained weight loss, or systemic symptoms) Yes Yes Clinical or radiologic suspicion of infection (e.g., end plate destruction on plain radiographs, history of drug or alcohol abuse, or systemic symptoms) Yes No Severe low back pain or radicular pain that is unresponsive to conservative therapy and with indications for surgical intervention Yes No Bone tumors (to detect or characterize) No Yes Advantages
Better visualization of soft tissue pathology
Better soft tissue contrast
Better visualization of neurologic structures
Improved sensitivity for cord pathology and for intrathecal masses
Improved sensitivity for infection and neoplasm
No radiation exposure; therefore safer for women who are pregnant, especially in the first trimester
Better visualization of calcified structures
Direct visualization of fractures
Direct visualization of fracture healing and fusion mass
More accurate in the assessment of certain borderline or active benign tumors
More available and less costly
Better accommodation for patients weighing > 300 lbs and for patients with claustrophobia
Less sensitive to patient motion; particularly useful for patients who cannot lie still or for patients who cannot cooperate for MRI

Diagnostic interventional techniques
Evidence-based interventional diagnostic techniques for low back pain are as follows:
▪ Facet joint blocks
▪ Discography
▪ Transforaminal epidural injections or selective nerve root blocks
▪ Sacroiliac joint injections
Pain provocation in any structure is an unreliable criterion, except in provocative discography. Relief of pain is an essential criterion in almost all structures. Most pain-provocative or pain-relieving tests used to diagnose painful conditions of the spine are more closely related to a physical examination than to a laboratory test.
For an anatomic structure to be deemed a potential cause of back pain it must fulfill the following four criteria developed by Bogduk [2] :
▪ It must have a nerve supply.
▪ It should be capable of causing pain similar to that seen clinically in normal volunteers.
▪ It must be susceptible to painful diseases or injuries.
▪ It must be demonstrated as a source of pain by diagnostic techniques of known reliability and validity.
The following three assumptions related to diagnostic use of neural blockade were developed by Hildebrandt [3] :
▪ The pathology causing pain is located in an exact peripheral location, and impulses from this site travel via unique and consistent neural routes.
▪ The injection of local anesthetic totally abolishes the sensory function of intended nerves.
▪ The relief of pain after local anesthetic block is attributable solely to the block of the target afferent neural pathway.
The limitations of the validity of these assumptions are (1) the complexities of anatomy, physiology, and the psychology of pain perception and (2) the effect of local anesthetics on impulse conduction
Ideally, a diagnostic block achieves block of the same structure three times as described below:
▪ All controlled blocks should include placebo injections of normal saline , but it may be neither logical nor ethical to use placebo injection of normal saline in conventional practice in each and every patient.
▪ As an alternative, the use of comparative local anesthetic block , on two separate occasions, during which the same structure is anesthetized using two local anesthetics with different durations of action, has been proposed.
The minimum requirements for performance of diagnostic interventional techniques are as follows:
▪ History and physical examination
▪ Informed consent
▪ Appropriate documentation of the procedure
▪ Correct environment, including a sterile operating room or procedure room, appropriate monitoring equipment, radiology equipment, sterile preparation, resuscitative equipment, needles, gowns, injectable drugs, intravenous fluids, anxiolytic medications, and trained personnel for preparation and monitoring of patients
Contraindications to the performance of a diagnostic interventional technique are as follows:
▪ Ongoing bacterial infection
▪ Possible pregnancy
▪ Bleeding diathesis and anticoagulant therapy
The reliability and validity of any diagnostic technique are determined by the following factors:
False-positive rate: The rate at which patients without a condition nonetheless have a positive test result.
False-negative rate: The rate at which patients with a condition nonetheless show a negative test result.
Placebo response: A remarkable phenomenon in which a placebo – a fake treatment, an inactive substance – can sometimes improve a patient’s condition simply because the person has the expectation that it will be helpful.
Sensitivity: A description of the diagnostic technique in relation to the prevalence of false-positive results; the most sensitive test yields a positive result for all cases in which the disease is present.
Specificity: A description of the diagnostic technique in relation to the prevalence of the false-negative results; the specificity is greatest when there is a positive test result only when the disease is present.

Facet or Zygapophyseal Joint Block
Diagnostic blocks of facet or zygapophyseal joint can be performed by anesthetizing the joint itself or the medial branches which supply the target joint with injections of local anesthetic, to test whether the joint is the source of pain ( Table 1.18 ). If pain is not relieved, the joint cannot be considered the source of pain. If pain is relieved, the joint may be considered the primary source of the pain.

Table 1.18 Possible Results of Diagnostic Block of Facet Joints
False-positive rates for diagnostic block of facet joints are shown in Table 1.19 , in comparison with rates at which facet joints are actually the source of chronic spinal pain. The false-negative rate, which is 8% at all spine levels, is due to unrecognized intravascular injection of local anesthetic.
Table 1.19 Accuracy of Diagnostic Block of Facet Joints: False-Positive Rate versus Rate of Facet Joint–Caused Chronic Spinal Pain Region of Spine Reported False-Positive Rates (%) Rate for Confirmed Facet Joint–Caused Chronic Spinal Pain (%) Cervical 27-63 54-67 Thoracic 55-58 42-48 Lumbar 17-47 15-45
Modified from Manchikanti L, Boswell MV, Singh V, Pampati V, Damron KS, Beyer CD. Prevalence of facet joint pain in chronic spinal pain of cervical, thoracic, and lumbar regions. BMC Musculoskelet Disord 2004;5:15.
The prevalence of facet joints as the source of chronic spinal pain is 30% in individuals younger than 65 years and 52% in older individuals, 38% in men, and 43% in women
The rationale for using facet joint blocks for diagnosis is based on the following findings in normal volunteers ( Figs 1-6 ):
▪ Cervical facet joints have been shown to be capable of being a source of neck pain and referred pain in the head or upper limb girdle.
▪ Thoracic facet joints have been shown to be capable of being a source of thoracic pain and referred pain over the chest wall.
▪ Lumbar facet joints have been shown to be capable of being a source of LBP and referred pain in the lower limb.

Figure 1–6 The main distribution of referred pain from each joint and the dorsal rami, as explained in the table. 1, occipital region; 2, upper posterolateral cervical region; 3, upper posterior cervical region; 4, middle posterior cervical region; 5, lower posterior cervical region; 6, suprascapular region; 7, superior angle of the scapula; 8, midscapular region; 9, shoulder joint; 10, upper arm.
Source Region Joint Main Region(s) of Pain Distribution C0-C1 2 C1-C2 2 C2-C3 3 C3-C4 3, 4 C4-C5 4, 5, 6 C5-C6 5, 6 C6-C7 7, 8 C7-T1 7, 8 Dorsal Ramus Region(s) to which Pain is Referred with Electrical Stimulation C3 1, 3 C4 4 C5 5 C6 7 C7 7,8
(Modified from Fukui S, Ohseto K, Shiotani M, Ohno K, Karasawa H, Naganuma Y, Yuda Y. Referred pain distribution of the cervical zygapophyseal joints and cervical dorsal rami. Pain 1996;68:79-83.)
Facet joint pain is neither an articular disorder nor a neurologic disorder. It does not meet the criteria for pain from other joints, which is typically diagnosed on the grounds of swelling, tenderness, and restricted motion. The referral patterns described for various joints are not only variable but also restricted. Other structures in the same segment, such as the disc, may produce the same pattern of pain. Most maneuvers used in physical examination are likely to stress several structures simultaneously, especially the disc, muscles, and facet joints, thus failing to provide any reasonable diagnostic criteria.
Most published studies have not found a correlation between facet joint–caused pain and imaging findings, including findings of MRI, CT, dynamic bending films, single-photon emission computed tomography (SPECT), and radionuclide bone scanning. Thus, controlled diagnostic blocks using two separate local anesthetics (or with placebo control) are the only means of confirming diagnosis of facet joint pain.

Safety and Complications
Complications of diagnostic block of the facet or zygapophyseal joint that are related to needle placement and drug administration are as follows:
▪ Dural puncture
▪ Spinal cord trauma
▪ Infection
▪ Intravascular injection
▪ Spinal anesthesia
▪ Chemical meningitis
▪ Neural trauma
▪ Pneumothorax
▪ Hematoma formation
Complications related to administration of steroids are as follows:
▪ Radiation exposure
▪ Facet capsule rupture
▪ Vertebral artery damage
▪ Local anesthetic leakage out of the joint into spinal canal
Another potential complication is an incidental block of the third occipital nerve, which may result in transient ataxia and unsteadiness due to partial blockade of the upper cervical proprioceptive afferents and the righting response, and phrenic nerve block, which can result from diagnostic block at the C3-C4, C4-C5, or C5-C6 facet joint block.

Provocative Discography
Provocative discography is a diagnostic procedure designed to determine whether a disc is intrinsically painful. It involves making the nucleus pulposus of an intervertebral disc opaque to render it visible on radiographs. The procedure involves disc puncture, disc stimulation, assessment of disc morphology, and assessment of the patient’s pain response.
The overall accuracy of the various modalities of provocative discography is as follows [4] :
▪ CT discography: 87%
▪ CT/myelography: 77%
▪ CT: 74%
▪ Myelography: 70%
▪ Discography alone: 58%

Safety and Complications
Complications of provocative discography are as follows:
▪ Infection: acute epidural abscess, subdural empyema, prevertebral abscess, and discitis
▪ Neural and spinal cord trauma
▪ Intravascular penetration, which may lead to post-injection hematoma
▪ Headache
The incidence of discitis is 2% to 3% for a single-open-needle technique but only 0.7% for a double-open-needle technique [4] .

Transforaminal Epidural Injections or Selective Nerve Root Blocks
The result of transforaminal epidural injection or selective nerve root block is positive when both of following conditions meets:
▪ Concurrent symptoms can be reproduced during root stimulation
▪ Full relief is attained after anesthetic infusion
This procedure is effective in evaluating patients with multilevel pathology to ascertain the source of their pain.

Safety and Complications
Complications of transforaminal epidural injections or selective nerve root blocks are as follows:
▪ Dural puncture
▪ Infection
▪ Vascular gas embolism
▪ Cerebral thrombosis
▪ Epidural hematoma
▪ Neural or spinal cord damage
▪ Complications related to administration of steroids

Sacroiliac Joint Blocks
Common sources of sacroiliac joint pain are as follows:
▪ Degenerative processes
▪ Repetitive shear or torsional forces to the joint as occurs in sports such as figure skating, golf, and bowling
▪ Trauma related to sudden heavy lifting, prolonged lifting and bending, torsional strain, rising from a stooped position, fall onto a buttock, or rear-end motor vehicle accident with the ipsilateral foot on the brake
▪ Disorders that may involve the sacroiliac joint, such as hyperparathyroidism, fracture, Reiter syndrome, psoriatic arthritis, ankylosing spondylitis, rheumatoid arthritis, and septic sacroiliitis

Safety and Complications
Complications of sacroiliac joint blocks are as follows:
▪ Infection
▪ Trauma to the sciatic nerve
▪ Other complications related to drug administration

Therapeutic interventional techniques
The rationale for therapeutic interventional techniques in the spine is based on the following considerations:
▪ Cardinal sources of chronic spinal pain, namely discs and joints, are accessible to neural blockade.
▪ Removal or correction of structural abnormalities of the spine may fail to cure and may even worsen painful conditions.
▪ Degenerative processes of the spine and the origin of the spine pain are complex.
▪ The effectiveness of a large variety of the therapeutic interventions in managing chronic spinal pain has not been demonstrated conclusively.
Interventional techniques in the management of chronic spinal pain include neural blockade and minimally invasive surgical procedures such as:
▪ Epidural injections
▪ Facet joint injections
▪ Neuroablation techniques
▪ Intradiscal neural therapy
▪ Disc decompression
▪ Morphine pump implantation
▪ Spinal cord stimulation
The requirements for the performance of therapeutic interventional techniques in the spine include:
▪ A sterile operating room or a procedure room
▪ Monitoring equipment
▪ Radiographic equipment
▪ Special equipment specific to technique
▪ Sterile preparation with all of the following available: resuscitative equipment, needles, gowns, agents for injection, intravenous fluids, sedative agents, and trained personnel for preparation and monitoring of the patient
Minimum requirements in preparation for these procedures are as follows:
▪ History and physical examination
▪ Informed consent
▪ Appropriate documentation of the procedure
Contraindications to therapeutic interventional techniques in the spine are as follows:
▪ Bacterial infection
▪ Possible pregnancy
▪ Bleeding diathesis and anticoagulant therapy

Facet Joint Injections
The effectiveness of intra-articular injections, medial branch blocks, and neurolysis of medial branches for pain relief over the short or long term is shown in Table 1.20 .
Table 1.20 Duration of Effectiveness of Therapeutic Interventional Techniques in Facet Joint Pain Modality Short-Term Long-Term Intra-articular injection ≤ 3 months 3 to 6 months Medial branch block ≤ 3 months 3 to 6 months Neurolysis of medial branches 3 to 6 months > 6 months

Epidural Injections
The three approaches for the epidural space are interlaminar, caudal, and transforaminal. The advantages and disadvantages of the three approaches are listed in Table 1.21 . The known evidence for the short-term or long-term effectiveness of epidural injections is summarized in Table 1.22.

Table 1.21 Advantages and Disadvantages of the Three Approaches to Injection of the Epidural Space
Table 1.22 Known Evidence for Effectiveness of Epidural Injections Type of Injection Short-Term Effect (Significant Relief ≤ 3 Months) Long-Term Effect (Significant Relief > 3 Months) Interlaminar Moderate evidence Limited evidence Caudal Strong evidence Moderate evidence Transforaminal Strong evidence Strong evidence

Safety and Complications
The complications of epidural injection related to needle placement are as follows:
▪ Dural puncture
▪ Spinal cord trauma
▪ Infection
▪ Hematoma formation
▪ Abscess formation
▪ Subdural infection
▪ Intracranial air injection
▪ Epidural lipomatosis
▪ Pneumothorax
▪ Nerve damage
▪ Headache
▪ Brain damage
▪ Increased intracranial pressure
▪ Intravascular injection
▪ Vascular injury
▪ Cerebral vascular or pulmonary embolism
The complications of epidural injection related to corticosteroid administration are as follows:
▪ Suppression of the pituitary adrenal axis
▪ Hypercorticism
▪ Cushing syndrome
▪ Osteoporosis
▪ Avascular necrosis of bone
▪ Steroid myopathy
▪ Epidural lipomatosis
▪ Weight gain
▪ Fluid retention
▪ Hyperglycemia

Epidural Adhesiolysis
The purpose and goals of percutaneous epidural lysis of adhesions are:
▪ To eliminate the deleterious effects of scar formation, which can physically prevent direct application of drugs to nerves or other tissues for treatment of chronic back pain.
▪ To ensure delivery of high concentrations of injected drugs to the target areas.
▪ To achieve epidural lysis of adhesions and direct deposition of corticosteroids in the spinal canal with the three-dimensional view provided by epiduroscopy or spinal endoscopy.
The known evidence for short-term or long-term effects of percutaneous epidural adhesions and spinal endoscopic adhesiolysis is summarized in Table 1.23.
Table 1.23 Known Evidence for Effectiveness of Percutaneous Epidural Adhesions and Spinal Endoscopic Adhesiolysis Percutaneous epidural adhesions
Moderate evidence for short-term effect (≤ 3 months)
Moderate evidence for long-term effect (3 to 6 months) with repeat interventions Spinal endoscopic adhesiolysis
Moderate evidence for short-term effect (3 to 6 months)
Limited evidence for long-term effect (> 6 months)

Safety and Complications
The complications of percutaneous epidural lysis of adhesions are as follows:
▪ Dural puncture, spinal cord compression, infection, steroids, hypertonic saline, hyaluronidase, and damage by the endoscope
▪ Administration of high volumes of fluids, potentially resulting in excessive epidural hydrostatic pressures (which may cause spinal cord compression, excessive intraspinal and intracranial pressure, epidural hematoma, bleeding, infection, increased intraocular pressure with resultant visual deficiencies, and even blindness and dural puncture)
▪ Unintended subarachnoid or subdural puncture with injection of local or hypertonic saline
▪ Catheter shearing and retention in the epidural space
▪ Excessive intraspinal pressure development with potential to affect both local and distant profusion, resulting in visual changes, even blindness
▪ A combination of high volumes of fluid and generation of high hydrostatic pressures (spinal endoscopic adhesiolysis > percutaneous epidural catheter adhesiolysis)
▪ Spinal cord trauma or spinal cord or epidural hematoma formation

Intradiscal Therapies
The known evidence for the short-term or long-term effects of epidural injections is described in Table 1.24.
Table 1.24 Evidence for Effectiveness of Intradiscal Therapies Intradiscal electrothermal therapy
Moderate evidence for short-term relief
Limited evidence for long-term relief Percutaneous disc decompression (PDD) Limited evidence for the effectiveness Nucleoplasty Limited evidence for the effectiveness

Intradiscal Electrothermal Therapy
Intradiscal electrothermal therapy (IDET) is performed by the introduction of a flexible catheter containing a resistive coil into the disc and thermal transmission for neural tissue damage. The primary indication for IDET is the presence of axial symptoms not indicating radicular pain.

Safety and complications
Complications related to intradiscal electrothermal therapy are as follows:
▪ Catheter breakage
▪ Nerve root injuries
▪ Postprocedure disc herniation at the treated level
▪ Cauda equina syndrome

Percutaneous Disc Decompression
In percutaneous disc decompression with nucleoplasty, radiofrequency energy is used to dissolve nuclear material. This reduction in volume of disc material results in lower intradiscal pressure. Bipolar radiofrequency coagulation further denatures proteoglycans, changing the internal environment of the affected nucleus pulposus, which leads to changes in intradiscal pressure.

Safety and complications
The complications of percutaneous disc decompression are as follows:
▪ Neural trauma
▪ Cauda equina syndrome and other neurologic complications

Implantable Therapies

Spinal Cord Stimulation
Brief history related to spinal cord stimulation
▪ The gate control theory by Melzack and Wall (1965) [9]
▪ Shealy’s the first spinal cord stimulator device for the treatment of chronic pain (1967) [8]
The mechanism of action of spinal cord stimulation occurs (1) at the local and supraspinal levels and (2) through dorsal horn interneuronal and neurochemical mechanisms. The indications for and contraindications to spinal cord stimulation are listed in Table 1.25. There is moderate evidence for long-term relief with spinal cord stimulation in a properly selected population with neuropathic pain.
Table 1.25 Indications for and Contraindications to Spinal Cord Stimulation Indications (for patients with chronic pain of predominantly neuropathic origin and topographical distribution involving the extremities)
In United States:
Failed back surgery syndrome
Complex regional pain syndrome type I and II
In Europe:
Chronic intractable angina and pain
Disability due to peripheral vascular disease Contraindications (such asprimary nociceptive conditions)
Degenerative disc disease
Sacroiliac dysfunction
Arthritis
Cancer
Acute tissue injury
Falowski S, Celii A, Sharan A. Spinal cord stimulation: an update. Neurotherapeutics 2008; 5: 86-99.

Complications
Complications of spinal cord stimulation range from simple, easily correctable problems, such as lack of appropriate paresthesia coverage, to devastating complications, such as paralysis, nerve injury, and death. Possible infections range from simple infections at the surface of a wound to epidural abscess and concomitant meningitis. Mechanical complications of the procedure are malposition, migration, breakage, and failure of the electrode lead.

Implantable Intrathecal Drug Administration Systems
The advantages and disadvantages of implantable intrathecal drug administration systems are listed in Table 1.26 . There is moderate evidence for long-term effectiveness of intrathecal infusion systems.
Table 1.26 Advantages and Disadvantages of Implantable Intrathecal Drug Administration Systems Advantages
More powerful analgesia at a significantly lower dose of administered drug
More consistent analgesia with a lower incidence of somnolence, mental clouding, constipation, and euphoria
Theoretically better for treatment of the chemically dependent patient with an intractable nociceptive and/or neuropathic pain condition (the intrathecal medication does not produce euphoria and cannot be manipulated by the patient) Disadvantages
Surgical risks involved with any implanted device
Risk of spinal injury from the catheter or infused medications
Risk of side effects specific to intrathecal drug delivery
High cost

Safety and complications
The most common immediate problems of implantable intrathecal drug administration (occurring at a rate of 20%) are as follows:
▪ Post–dural puncture headache
▪ Infection
▪ Nausea
▪ Urinary retention
▪ Pruritus
Long-term complications of the modality include:
▪ Failure of the catheter (10%-40%) and pump failure (somewhat lower rate)
▪ Granuloma
Commonly reported drug-related complications are as follows:
▪ Pedal edema with a central effect on antidiuretic hormone
▪ Hormonal changes resulting in decreases in libido and sexual dysfunction
▪ Changes in testosterone levels in men that cause fatigue as well as loss of body hair and sex drive

Medical decision-making – spinal pain
The key components for establishing a diagnosis and/or selecting a management option (medical decision-making) in the patient with spinal pain are as follows:
1. Consider all of the many options for diagnosis and management.
2. Obtain, review, and analyze all medical records, diagnostic tests, and other information.
3. Consider the risk of significant complications as well as the morbidity and mortality of diagnostic procedures and/or possible management options; also consider the risks of any comorbidities in patients presenting with spinal pain.
Treatment for spinal pain is medically necessary when the following conditions are met:
▪ Suspected organic problem
▪ Nonresponsiveness to less invasive modalities of treatments
▪ Pain and disability of moderate to severe degree
▪ No evidence of contraindications, such as severe spinal stenosis resulting in intraspinal obstruction, infection, and predominantly psychogenic pain
▪ Responsiveness to prior interventions with improvement in physical and functional status

Activity recommendations for acute lower back pain
Patients with acute LBP should be advised to stay active and continue ordinary activity within limits permitted by the pain. Compared with bed rest and back-mobilizing exercises, remaining active leads to:
▪ More rapid recovery
▪ Less chronic disability
▪ Fewer recurrent problems

Activity Modification

▪ Patients should be advised to continue routine activity while paying attention to correct posture.
▪ Those with acute LBP problems may be more comfortable if they temporarily limit or avoid specific activities known to increase mechanical stress on the spine, especially prolonged unsupported sitting, heavy lifting, and bending or twisting the back, particularly while lifting.
▪ Activity recommendations for the employed patient with acute low back symptoms must take into consideration the patient’s age and general health and the physical demands of the patient’s job.
▪ Patients should discontinue any activity or exercise that causes spread of symptoms ( peripheralization ).

Bed Rest

▪ Bed rest is not recommended. If the patient must rest, bed rest should be limited to no more than 2 days and should be regarded as an option only for patients with severe initial symptoms of primarily leg pain [6] .
▪ A gradual return to normal activities is more effective and leads to more rapid improvement with less chronic disability than prolonged bed rest for treatment of acute low back problems.
▪ Prolonged bed rest—4 days or longer—may lead to debilitation and is not recommended for treatment of acute low back problems.

Exercise
Patients should discontinue any activity or exercise that causes spread of symptoms (peripheralization). Low-stress aerobic and flexibility exercises can prevent debilitation due to inactivity during the first month of symptoms and thereafter may help return patients to the highest level of functioning appropriate to their circumstances. Recommendations that involve gradually increasing exercise quotas have better outcomes than telling patients to stop exercising if pain occurs. Most patients with acute low back problems can begin aerobic (endurance) programs that minimally stress the back (walking, biking, or swimming) during the first 2 weeks.
Strengthening exercises for trunk muscles (especially back extensors), with gradual increase, are helpful for patients with low back problems. During the first 2 weeks, however, strengthening exercises may aggravate symptoms because they mechanically stress the back more than endurance exercise. It is important for patients to consult with a medical specialist such as a qualified spine specialist, who can evaluate individual symptoms and recommend a safe and effective program. Self-treatment with an exercise program not specifically designed for the patient may aggravate the symptoms.
A self-care brochure can be given to the patient to emphasize the following issues:
▪ It is likely that the patient does not have serious disease if the doctor found no “red flag” symptoms.
▪ Hurt does not equal harm.
▪ There is a good prognosis for LBP. The majority of patients experience significant improvement in 2 to 4 weeks.
▪ Bed rest is not recommended and should be limited to no more than 2 days.
▪ Light activity will not further injure the spine and typically helps speed recovery.
▪ A progressive resumption of work and activity levels leads to better short-term and long-term outcomes.
▪ Information and advice regarding any specific potentially painful activities, such as sitting, lifting, and getting up from bed should be included.
▪ No specific exercise type can be recommended as more effective than any other.
Examples of specific advice are:
1. Exercise as soon as back pain allows.
2. Minimize bed rest, keep mobile, and increase walking time each day.
3. Some of the easier activities to resume or begin after an episode of back pain are walking and swimming.

Follow-up Visit for Acute Lower Back Pain
Because most patients with acute pain improve by 2 weeks, a conservative treatment approach, as previously described, is recommended. Patients whose LBP is not improving or who experience significant limitation of daily activity at home or work should contact their provider within 1 to 3 weeks of the initial evaluation . Patients who are improving should continue home self-care.
Red flags and psychosocial indicators ( yellow flags ) should be reviewed and evaluated for at each contact or visit. Indications for referral to superior hospital or institution include:
▪ Failure to make improvement with home self-care after 2 weeks
▪ Severe incapacitating and disabling back or leg pain
▪ Significant limitation of functional or job activities

General decision-making process for chronic low back pain and sciatica

Chronic Low Back Pain
Reevaluation, including a general assessment, should be performed for patients not improving after 6 weeks (chronic LBP). The assessment should include a subjective pain rating , a functional assessment , and a clinician’s objective assessment . Psychosocial screening and assessment tools should be used to rule out major depression in adults in primary care.
Of the 10% of patients with chronic symptoms, 90% have chronic LBP and only 10% have chronic sciatica. For patients not improving after 6 weeks, lumbar spine radiographs , as described later, should be obtained.
Physical factors that may lead to delayed recovery or prolonged disability include malignancy, infection, metabolic, and biomechanical conditions (e.g., sacroiliac joint dysfunction). Blood testing, including a complete blood count and measurement of the erythrocyte sedimentation rate, should be ordered if there is suspicion of cancer or infection.
The patient should be evaluated for sacroiliac joint dysfunction . Clinical indicators of the disorder include delayed recovery with unilateral pain below L5, pain near the posterior-superior iliac spine, and, sometimes, radicular or referred pain to the groin or thigh, or below the knee. Pain from the sacroiliac joint can often be referred into the lower extremity, even below the knee or into the foot. The most reliable locations are below L5, in the region of the posterior-superior iliac spine, and into the groin. Diagnostic maneuvers for this condition are the Patrick test, the gapping test, the compression test, and the Gaenslen test. Appropriate treatment of sacroiliac joint dysfunction by a trained spine professional involves manual therapy, instruction on self-corrective maneuvers, and strengthening exercises. There is at least some theoretical support for active rehabilitation of the abdominal musculature to stabilize the joint in the treatment of sacroiliac joint dysfunction.
Lumbar spine radiographs (anteroposterior and lateral views) should be obtained if indicated. Oblique views are not recommended; they add only minimal information in a small percentage of cases, and they more than double the radiation exposure for the patient. Several radiographic findings are of questionable clinical significance and may be unrelated to back pain; they include the following [7] :
▪ Single disc space narrowing
▪ Spondylolysis
▪ Lumbarization
▪ Sacralization
▪ Schmorl nodes
▪ Spinal bifida occulta
▪ Disk calcification
▪ Mild to moderate scoliosis

Chronic Sciatica
MRI and CT are not useful during acute sciatica unless there are red flag indications and the patient is a potential surgical candidate. In isolated cases of LBP without radicular symptoms, MRI is the preferred diagnostic procedure. However, in an otherwise healthy adult suffering LBP with radicular symptoms who has not undergone a previous back surgery, a CT scan may be as sensitive as an MR image (see Table 1.17 ).

Treatment of the painful motion segment
Diagnosis of radiographic cervical instability requires either of the following findings:
▪ Sagittal displacement greater than 3 mm or relative sagittal plane displacement greater than 11% on a plain film of the spine in the neutral position
▪ Sagittal plane translation greater than 3.5 mm or rotation greater than 20% on a flexion-extension film
Indications for fusion of the degenerative spine are listed in Table 1.27 :
Table 1.27 Indications for Fusion Procedures of the Degenerative Spine Procedure Absolute Indications Controversial Indications Cervical spine:     Anterior infusion Posterior fusion
Unstable
> 3 mm movement
> 11° range of motion
Kyphosis
After laminectomy in the kyphotic spine
Bilateral facetectomy
Straightening of the spine
Axial neck pain
After discectomy
After laminectomy in straightened spine
Sustained axial pain after laminectomy Lumbar spine
Decompression with grade II or greater spondylolisthesis
After repeated (> 2) discectomies
Radiographically documented instability (defined as > 3 mm movement and translational movement and/or movement > 10 degrees on flexion-extension radiographs)
After bilateral facetectomy
Decompression with grade I spondylolisthesis
Suggestive mechanical pain
After unilateral facetectomy
Bambakidis NC, Feiz-Erfan I, Klopfenstein JD, Sonntag VK. Indications for surgical fusion of the cervical and lumbar motion segment. Spine 2005; 30 (16 Suppl): S2-S6.
Indications for surgical decompression and fusion in the cervical spine are as follows:
▪ Radiographic evidence of instability with progressive neurologic deterioration
▪ Mild disabling myelopathy
▪ Moderate to severe myelopathy
Fusion is universally indicated if an anterior approach is used. Fusion after posterior laminectomy is controversial but is indicated in the presence of a deformity or preoperative reversal of the lordotic curvature.
Indications for cervical arthroplasty are as follows:
▪ Radiculopathy caused by disc herniation
▪ Radiculopathy caused by foraminal osteophytes
▪ Myelopathy caused by disc herniation
The advantages of lumbar interbody fusion over posterolateral fusion are as follows:
▪ Interbody grafts are compressed by 80% of spinal loads, whereas posterolateral grafts are compressed by 20% of spinal loads ( Fig. 1-7 ).
▪ Interbody grafts occupy 90% of intervertebral body surface area, whereas posterolateral grafts occupy 10% of intervertebral bony surface area.
▪ The interbody space is more vascular than the posterolateral space, thereby promoting the chances for fusion.
▪ Interbody grafts can better restore coronal and sagittal balance.
▪ Interbody fusions may be promoted by the use of recombinant human bone morphogenetic hormone type 2 (rhBMP-2) in the disc space.
▪ Differentiation of fusion and pseudarthrosis is easier with an interbody fusion than with a posterolateral fusion.

Figure 1–7 Illustration of spinal loads and articular surface area across the lumbar spinal column.
Potential indications for posterolateral lumbar fusion are as follows:
1. Clinical or radiographic spinal instability due to:
a. Trauma.
b. Scoliosis.
c. Neoplasm.
d. Infection.
e. Degeneration.
f. Deformity correction.
2. Spondylolisthesis demonstrating:
a. Documented progression.
b. Symptomatic grade I/II slip refractory to conservative therapy.
c. Grade III/IV slip.
3. Degenerative disc disease causing discogenic LBP.
4. Recurrent lumbar disc herniation with significant mechanical back pain.
5. Third or greater recurrence of lumbar disc herniation with radiculopathy (with or without back pain).
6. Treatment of pseudoarthrosis.
Potential indications for lumbar interbody fusion are as follows:
▪ Spondylolisthesis with documented progression and/or symptomatic grade I/II slip refractory to conservative therapy
▪ Degenerative disc disease causing discogenic LBP
▪ Recurrent lumbar disc herniation with significant mechanical LBP
▪ Postdiscectomy collapse with neuroforaminal stenosis and secondary radiculopathy
▪ Third or greater recurrence of lumbar disc herniation with radiculopathy (with without back pain)
▪ Pseudoarthrosis
▪ Postlaminectomy kyphosis
▪ Lumbar deformity with coronal and/or sagittal plane imbalance
Table 1.28 compares posterolateral fusion with lumbar interbody fusion.
Table 1.28 Indications for the Selection of Posterolateral Fusion versus Lumbar Interbody Fusion Posterolateral fusion
No risk factors for pseudoarthrosis
Osteopenia
Grade III/IV spondylolisthesis
Alignment/balance preserved Lumbar interbody fusion
Risk factors for pseudoarthrosis (e.g., tobacco use, rheumatologic disease, diabetes)
Axial load-bearing pain
Need to correct coronal/sagittal imbalance
Table 1.29 lists the relative contraindications to lumbar fusion procedures.
Table 1.29 Relative Contraindications to Lumbar Fusion Surgery Contraindication To Posterolateral Fusion To Lumbar Interbody Fusion Multilevel (> 3 levels) degenerative disc disease (except in cases of spinal deformity) x x Single-level disc disease causing radiculopathy without symptoms of mechanical low back pain or instability x x Severe osteoporosis (possible subsidence of interbody grafts through the end plates)   x
Table 1.30 lists the appropriate uses for interbody grafts (spacers).
Table 1.30 Uses for Interbody Grafts Type Shape PEEK (polyetheretherketone) interbody spacer One boomerang spacer Carbon fiber cage One boomerang spacer Titanium cages Two small circular cages One small circular cage One boomerang cage One elliptical cage Allograft One “kidney bean–shaped” allograft Two circular allografts Macropore spacer One boomerang spacerOne or two circular or rectangular shaped spacers
Wang JC, Mummaneni PV, Haid RW. Current treatment strategies for the painful lumbar motion segment: posterolateral fusion versus interbody fusion. Spine. 200; 30(16 Suppl): S33-43.
Table 1.31 summarizes the inclusion and exclusion criterias for lumbar disc arthroplasty.
Table 1.31 Inclusion and Exclusion Criteria for Lumbar Disc Arthroplasty Trials Type of implant Inclusion Criteria Exclusion Criteria SB Charité III
Age 18-60 years
Failed nonoperative treatment of at least 6 months’ duration
Single-level degenerative disc disease at L4-L5 or L5-S1 confirmed by MRI and provocative discography
Oswestry Disability Index ≥ 30
Back pain Visual Analog Score ≥ 40
Previous thoracic or lumbar fusion
Multilevel degenerative disc disease
Facet joint arthrosis
Noncontained herniated nucleus pulposus
Osteoporosis
Spondylolisthesis > 3 mm
Midsagittal stenosis < 8 mm Prodisc II
Age 18-60 years
At least 6 months of failed nonoperative therapy
Degenerative disc disease (DDD) at one or two adjacent vertebral levels between L3 and S1, where a diagnosis of DDD requires 1. primary back and/or radicular pain 2. Radiographic confirmation of any one of the following by CT, MRI, discography, plain film, myelography and/or flexion/extension films: 1) lack of instability (defined as > 3mm of translation or > 5° of angulation) 2) Decreased disc height > 2mm 3) Scarring/thickening of the annulus fibrosus 4) herniated nucleus pulposus or 5) vacuum phenomenon
Oswestry Disability Index ≥ 40
Psychosocially, mentally, or physically able to fully comply with this protocol, including adhering to the follow-up schedule and requirements and the filling out of forms
> 2 degenerative levels
End plate dimensions < 34.5 mm in the coronal plane and/or < 27 mm in the sagittal plane
Known allergy to titanium, polyethylene, cobalt, chromium, or molybdenum
Prior lumbar fusion
Post-traumatic vertebral body compromise/deformity
Facet degeneration
Lytic spondylolisthesis or spinal stenosis
Degenerative spondylolisthesis of grade > 1
Back or leg pain of unknown etiology
Osteoporosis
Metabolic bone disease (excluding osteoporosis, e.g., Paget’s disease)
Morbid obesity (BMI > 40 or weight > 100 lb over ideal body weight)
Pregnant or interested in becoming pregnant in the next 3 years
Active systemic/local infection
Medications or drugs known to potentially interfere with bone/soft tissue healing, excluding smoking
Rheumatoid arthritis or other autoimmune spondyloarthropathies
Systemic disease, including but limited to acquired immunodeficiency syndrome, human immunodeficiency virus, hepatitis
Active malignancy: a patient with a history of any invasive malignancy (except non-melanoma skin cancer), unless he/she has been treated with curative intent and there has been no clinical signs or symptoms of the malignancy for at least 5 yr
Issues to be considered in the selection of lumbar spinal fusion for the treatment of disc herniation and radiculopathy are as follows:
▪ Lumbar spinal fusion is not recommended as routine treatment after primary disc excision in the patient with a herniated lumbar disc that was causing radiculopathy.
▪ Lumbar spinal fusion is recommended as a potential surgical adjunct in the patient with a herniated disc in whom there is evidence of preoperative lumbar spinal deformity or instability and in the patient with significant chronic axial LBP associated with radiculopathy due to a herniated lumbar disc.
▪ Reoperative discectomy is recommended as treatment option in the patient with a recurrent lumbar disc herniation.
▪ Reoperative discectomy combined with fusion is recommended as a treatment option in the patient with a recurrent disc herniation associated with lumbar instability, deformity, or chronic axial LBP.
▪ Pedicle screw fixation may be used as an adjunct to lumbar posterolateral fusion (see below). Considerations in the selection of fusion after decompression to treat patients with stenosis without spondylolisthesis are as follows:
▪ In situ posterolateral lumbar fusion is not recommended as a treatment option in the patient with lumbar stenosis in whom there is no evidence of preexisting spinal instability or likely iatrogenic instability after facetectomy.
▪ In situ lumbar posterolateral lumbar fusion is recommended as a treatment option in addition to decompression in patients with lumbar stenosis without deformity in whom there is evidence of spinal instability.
▪ The addition of pedicle screw instrumentation is not recommended in conjunction with posterolateral lumbar fusion after decompression for lumbar stenosis in the patient without spinal deformity or instability.
Issues to be considered in the selection of interbody techniques for lumbar fusion to treat degenerative disease of the lumbar spine are as follows:
▪ It is recommended that both posterolateral lumbar fusion and interbody fusion techniques — posterior, transforaminal, or anterior—be considered as treatment options for patients with LBP due to degenerative disk disease at one or two levels.
▪ Placement of an interbody graft is recommended as a treatment option to improve fusion rates and functional outcome in patients undergoing surgery for LBP due to degenerative disk disease at one or two levels. The surgeon is cautioned that the marginal improvement in fusion rates and functional outcome with these techniques is associated with higher complication rates, particularly when combined approaches are used.
▪ The use of multiple approaches (anterior or and posterior) to accomplish lumbar fusion is not recommended as a routine option for the treatment of patients with LBP without deformity.
Considerations in the selection of pedicle screw fixation as an adjunct to posterolateral fusion for treatment of LBP are as follows:
▪ Pedicle screw fixation is recommended as a treatment option for patients with LBP treated with posterolateral fusion who are at high risk for fusion failure, because the use of pedicle screw fixation improves fusion success rates.
▪ Pedicle screw fixation is not recommended as a routine adjunct to posterolateral fusion in the treatment of patients with chronic LBP due to degenerative disk disease, because there is conflicting evidence that the use of pedicle screw fixation is associated with high costs and complications.
The issues to be considered in the use of lumbar facet joint injections related to lumbar fusion surgery are as follows:
▪ The use of lumbar facet joint injection is recommended as a diagnostic tool for predicting the response to lumbar facet radiofrequency ablation.
▪ The use of lumbar facet joint injection is not recommended as a diagnostic tool to predict the response to lumbar fusion surgery.
Considerations for the use of brace therapy as an adjunct to or substitute for lumbar fusion are as follows :
▪ Lumbar braces are recommended as a means of decreasing the number of sick days lost due to LBP among workers with previous lumbar injury.
▪ Lumbar braces are not recommended as a means of decreasing LBP in the general working population.
▪ The use of lumbar brace therapy as a preoperative diagnostic tool to predict the outcome of lumbar fusion surgery is not recommended .
▪ The use of transpedicular external fixation as a tool to predict the outcome of lumbar fusion surgery is not recommended .
Issues to be considered for the use of electrophysiologic monitoring during fusion procedures for degenerative disease of lumbar spine are as follows:
▪ Intraoperative evoked electromyography (EMG) response recording is recommended as an option during lumbar spinal fusion surgery when the operating surgeon desires immediate information about the integrity of the pedicle wall, because an intact pedicle wall produces a normal evoked EMG response.
▪ Intraoperative monitoring of somatosensory or dermatomal somatosensory evoked potentials, EMG, and/or evoked EMG responses are recommended only as adjunctive options during instrumented lumbosacral fusion procedures for degenerative spinal disease. The use of any of these modalities has not been convincingly demonstrated to influence patient outcome favorably.
Considerations for the use of autologous bone or rhBMP-2 bone graft substitute in fusion procedures for the degenerative disease of the lumbar spine are as follows:
▪ Recombinant human bone morphogenetic protein type 2 ( rhBMP-2 ) in combination with hydroxylapatite and tricalcium phosphate may be used as a substitute for autograft bone in some cases of posterior lumbar fusion.
▪ Several formulations of calcium phosphate are recommended as bone graft extenders, especially when used in combination with autologous bone.
Treatment guidelines for bone growth stimulators and lumbar fusion are as follows:
▪ Either direct current stimulation or capacitative coupled stimulation is recommended as an adjunct to spinal fusion to increase fusion rates in patients who are at high risk for arthrodesis failure after posterior lumbar fusion.
▪ Pulsed electromagnetic field stimulation is recommended as an adjunct to increase fusion rates in similar patients treated with lumbar interbody fusion procedures.

Cancer-related spinal pain
Figure 1-8 shows an algorithm for management of metastatic cancer–related spinal pain and the locations of primary neoplasms producing metastatic bone lesions are described in Table 1.32 .

Figure 1–8 Algorithm for management of metastatic cancer–related spinal pain.
Table 1.32 Location of Primary Neoplasms Producing Metastatic Bone Lesions Primary Site Number of Lesions (%) Breast 2020 (40) Lung 646 (13) Prostate 296 (6) Kidney 284 (6) Gastrointestinal tract 255 (5) Bladder 160 (3) Thyroid 110 (2) Total 5006
From Herkowitz, HN, Garfin SR, Eismont FJ, et al : Rothman-Simeone: The Spine, 5th ed. Philadelphia, Saunders, 2006, p. 1284.
Other information for cancer-related spinal pain is summarized such as incidence and prognosis of bone metastasis ( Table 1.33 ), radiologic appearance of metastatic bone lesions ( Table 1.34 ), predicting the risk of pathologic fracture ( Table 1.35), Karnofsky’s performance status ( Table 1.36 ), signs of spinal compression ( Table 1.37), categories of skeletal spinal metastasis ( Table 1.38), and Tokuhashi’s scoring system for spinal metastasis ( Table 1.39 ).

Table 1.33 Incidence and Prognosis of Bone Metastasis
Table 1.34 Radiologic Appearance of Metastatic Bone Lesions Radiologic Appearance Primary Lesion Osteolytic Lung, thyroid, kidney, colon Osteoblastic Prostate, bladder, stomach Mixed Breast

Table 1.35 Predicting the Risk of Pathologic Fracture
Table 1.36 Karnofsky Performance Status Grade Performance Level 100 Normal, no complaints, no evidence of disease 90 Able to carry on normal activity; minor signs or symptoms of disease 80 Normal activity with effect; some signs symptoms 70 Cares for self; unable to carry on normal activity or to do active work 60 Requires occasional assistance, but is able to care for most of his or her needs 50 Requires considerable assistances and frequent medical care 40 Disabled, requires special care and assistance 30 Severely disabled, hospitalization indicated; death not imminent 20 Very sick, hospitalization necessary, active supportive treatment necessary 10 Moribund, fatal processes, progressing rapidly 0 Dead

Table 1.37 Signs of Spinal Compression
Table 1.38 Categories of Skeletal Spinal Metastasis Category Severity of Skeletal Involvement by Metastasis I No major neurologic involvement II Involvement of bone without collapse and instability III Major neurologic involvement (sensory or motor) without significant bone involvement IV Vertebral collapse with pain caused by mechanical causes or instability but without significant neurologic impairment V Vertebral collapse or instability combined with major neurologic impairment
Modified from Herrington KD: Metastatic disease of the spine. J Bone Joint Surg Am 1986;68:1110-1115.
Table 1.39 Tokuhashi’s Scoring System for Spinal Metastasis Characteristic Point(s) General condition (performance status, PS):   Poor (PS 10-40%) 0 Moderate (PS 50-70%) 1 Good (PS 80-100%) 2 Number of extraspinal bone metastases foci:   ≥ 3 0 1-2 1 0 2 Number of metastases in the vertebral body:   ≥ 3 0 1-2 1 0 2 Metastases to the major internal organs:   Irremovable 0 Removable 1 No metastases 2 Primary site of cancer:   Lung, osteosarcoma, stomach, bladder, esophagus, pancreas 0 Liver, gallbladder, unidentified 1 Other Primary Sites 2 Kidney, uterus 3 Rectum 4 Thyroid, breast, prostate, carcinoid tumor 5 Palsy:   Complete (Frankel A, B) 0 Incomplete (Frankel C, D) 1 None (Frankel E) 2 Current Trend In Treatment According to Total Score 0-8: ≥ 6-8 months (actual survival period) Conservative treatment or palliative surgery 9-11: ≤ 6 months (actual survival period) Palliative or excisional surgery 12-15: ≤ 1 year (actual survival period) Excisional surgery
Modified from Tokuhashi Y, Matsuzaki H, Oda H, et al: A revised scoring system for preoperative evaluation of metastatic spine tumour prognosis. Spine 2005;30:2186-2191.

Differential diagnosis
Table 1.40 summarizes the differentiating features of the types and causes of low back pain.

Table 1.40 Differentiating Features of Low Back Pain

References

1. World Health Organization. International Classification of Diseases and Related Health Problems, 9th revision. Available at http://www.cdc.gov/nchs/icd/icd9.htm
2. Bogduk N. Low back pain. In Clinical Anatomy of Lumbar Spine and Sacrum , 4th ed, New York: Churchill Livingstone; 2005:183-216.
3. Hildebrandt J. Relevance of nerve blocks in treating and diagnosing low back pain—is the quality decisive. Schmerz . 2001;6:474-483. ? [in German]
4. Manchikanti L, Staats PS, Singh V, et al. Evidence-based practice guidelines for interventional techniques in the management of chronic spinal pain. Pain Physician . 2003;6:3-81.
5. Fraser RD, Osti OL, Vernon-Roberts B. Discitis after discography. J Bone Joint Surg Br . 1987;69:26-35.
6. van Tulder M, Becker A, Bekkering T, et al. COST B13 Working Group on Guidelines for the Management of Acute Low Back Pain in Primary Care: Chapter 3: European guidelines for the management of acute nonspecific low back pain in primary care. Eur Spine J . 2006;15(Suppl. 2):S169-S191.
7. Institute for Clinical Systems Improvement (ICSI). Adult Low Back Pain. Released 11/2008. Available at http://www.icsi.org/guidelines_and_more/gl_os_prot/musculo-skeletal/low_back_pain/low_back_pain__adult_5.html
8. Shealy CN, et al. Electrical inhibition of pain: experimental evaluation. Anesth Analg . 1967;46(3):299-305.
9. Melzack R, Wall PD. Pain mechanisms: a new theory. Science . 1965;150:971-979.
Chapter 2 Current Understanding of Spinal Pain and the Nomenclature of Lumbar Disc Pathology

Kyung-Hoon Kim, MD, PhD, Inn-Se Kim, MD, PhD
Any structure to be deemed a cause of back pain should:
▪ Have a nerve supply.
▪ Be capable of causing pain similar to that seen clinically, with this capability ideally demonstrated in normal volunteers.
▪ Be susceptible to diseases or injuries that are known to be painful.
▪ Have been shown to be a source of pain in patients through the use of diagnostic techniques of known reliability and validity.
Tissues capable of transmitting pain in the back are as follows:
▪ Common sources of spinal pain that can be confirmed as such by radiography, computed tomography (CT), magnetic resonance imaging (MRI), or electromyography (EMG)/nerve conduction velocity (NCV) testing include intervertebral discs, facet joints, spinal cord or nerve root dura, sacroiliac joints, and atlantoaxial and atlantooccipital joints.
▪ Common sources of spinal pain that are identified through medical history or a physical examination include vertebrae, muscles, fascia, and ligaments.

General pain mechanism
The two categories of pain are as follows:
▪ Spontaneous pain may be continuous or intermittent, superficial or deep, and may elicit different subjective sensations described as burning, shock-like, aching, and so on.
▪ Stimulus-evoked pain occurs in response to mechanical, thermal (cold and heat), or chemical, low- or high-intensity stimuli applied statically or dynamically to skin, joints, bone, muscle, or viscera.
Potential associations between particular mechanisms and particular symptoms are as follows:
▪ A reduced pain threshold to heat stimuli applied directly to a site of inflammation can be associated with peripheral sensitization.
▪ Tactile allodynia in a noninflamed area can be associated with an N -methyl- D -aspartate (NMDA) receptor–mediated central sensitization.
▪ Spontaneous burning pain can be associated with activity of C fibers.
▪ Paresthesia can be associated with activity of ectopic A fibers.
The pain evoked by different input channels represents operation of multiple mechanisms , such as the following:
Nociceptive transduction: Activation of high-threshold receptor–ion channel transducers in nociceptor peripheral terminals
Peripheral sensitization: Change in threshold sensitivity of receptor–ion channel transducers in nociceptor peripheral terminals
Altered sensory neuron excitability: Changes of the expression-phosphorylation-accumulation of ion channels in primary afferents
Central sensitization: Post-translational changes in ligand- and voltage-gated ion channel kinetics in central (spinal cord and brain) neurons, which change the neurons’ excitability and the strength of their synaptic inputs
Phenotype modulation: Alterations in the expression of receptors, transmitters, and/or ion channels in peripheral and central neurons
Synaptic reorganization: Modification of synaptic connections caused by cell death or sprouting
Disinhibition: Loss of local inhibition at different relay levels in the neuraxis and of descending inhibition originating in the forebrain and brainstem and terminating in the brain stem and spinal cord, caused by decreased activation of neurons, downregulation of receptors-transmitters, and cell death
A number of different input channels can lead to the pain sensation. These should be the first anatomic targets for treatment ( Fig. 2-1 ; Table 2.1 ), as follows:
▪ Nociceptive pain: Nociceptor activation in the periphery by noxious mechanical-thermal or chemical stimuli.
▪ Peripheral sensitization: Activation of sensitized nociceptors in the periphery by low-intensity stimuli.
▪ Peripheral nerve injury: Ectopic discharge in nociceptors originating at a neuroma, a dorsal root ganglion, a peripheral nerve, or a dorsal root.
▪ In combination with central sensitization, synaptic reorganization, or disinhibition: Low-intensity afferent activation in the periphery by low-intensity mechanical-thermal stimuli.
▪ Peripheral nerve injury associated with central sensitization, synaptic reorganization, or disinhibition: Ectopic discharge in low-threshold afferents originating at a neuroma, dorsal root ganglion, peripheral nerve and/or dorsal root.
▪ In the dorsal horn, thalamus, or cortex: Spontaneous activity in central neurons.

Figure 2–1 A diagrammatic representation of the relationships among the disease or injury, mechanisms, symptoms, and pain syndromes. The ideal for pain management is to treat the mechanisms apart from disease-modifying therapy.
(Adapted from Woolf CJ, Max MB: Mechanism-based pain diagnosis: Issues for analgesic drug development. Anesthesiology 2001;95:241-249.)

Table 2.1 Drug Treatment Based on Pain Mechanism Molecular Targets*
The four primary types of pain ( Fig. 2-2 ) are as follows:
Nociceptive pain: transient pain in response to a noxious stimulus
Inflammatory pain: spontaneous pain and hypersensitivity to pain in response to tissue damage and inflammation
Neuropathic pain: spontaneous and hypersensitivity to pain in association with damage to or a lesion of the nervous system (the symptoms of neuropathic pain are described in Box 2.1 )
Functional pain: hypersensitivity to pain resulting from abnormal central processing of a normal input

Figure 2–2 The four primary types of pain. A. Nociceptive pain: transient pain in response to a noxious stimulus, B. Inflammatory pain: spontaneous pain and hypersensitivity to pain in response to tissue damage and inflammation, C. Neuropathic pain: spontaneous and hypersensitivity to pain in association with damage to or a lesion of the nervous system, D. Functional pain: hypersensitivity to pain resulting from abnormal central processing of a normal input.
(From Woolf CJ: Pain: Moving from symptom control toward mechanism- specific pharmacologic management. Ann Intern Med 2004;140:441-451.)

BOX 2.1 Positive and Negative Symptoms of Peripheral Neuropathic Pain
Woolf CJ: Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy. Life Sci 2004;74:2605-2610.

Positive Symptoms

Spontaneous pain
Paresthesia
Dysesthesia
Allodynia
Hyperalgesia/hyperpathia

Negative Symptom

Loss of sensation
Adaptive pain and maladaptive pain are defined in Box 2.2 .

BOX 2.2 Two Broad Classes of Pain
Modified from Woolf CJ; American College of Physicians; American Physiological Society. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004;140:441-451.

Adaptive Pain
“The good”
Pain that contributes to survival by protecting the organism from injury or promoting healing when injury has occurred (nociceptive pain)
Coupled from a noxious stimulus or healing tissue

Maladaptive Pain
“The bad and the ugly”
An expression of the pathologic operation of the nervous system (neuropathic pain) or abnormal operation of the nervous system (functional pain)
Uncoupled from a noxious stimulus or healing tissue
Pain as disease
Multiple mechanisms that can produce pain, as follows:
Nociception: The sole mechanism that causes nociceptive pain and is comprised of the processes of transduction, conduction, transmission, and perception.
Transduction: The conversion of a noxious thermal, mechanical, or chemical stimulus into electrical activity in the peripheral terminals of nociceptor sensory fibers. This process is mediated by specific receptor ion channels expressed only by nociceptors ( Fig. 2-3 ).
Conduction: The passage of action potentials from the peripheral terminal along axons to the central terminal of nociceptors in the central nervous system.
Transmission: the synaptic transfer and modulation of input from one neuron to another ( Fig. 2-4 ).
Central sensitization: Contributes to inflammatory, neuropathic, and functional pain ( Figs. 2-3 and 2-5 ).

Figure 2–3 A, The peripheral terminal of a nociceptor sensory neuron. The different transducing receptor and ion channels that respond to thermal, mechanical, and chemical stimuli are shown. MDEG, mammalian degenerin; P2X, purinergic receptor; TRM3, 2’-O-ribose methyltransferase 3. B, The mechanism of peripheral sensitization. Inflammatory mediators, such as prostaglandin E 2 (PGE 2 ), bradykinin (BK), and nerve growth factor (NGF), activate intracellular kinases in the peripheral terminal that phosphorylate transducer channels to reduce their threshold or sodium channels to increase excitability. C, Transcriptional changes in the dorsal root ganglion (DRG). Activity, growth factors, and inflammatory mediators act on sensory neurons to activate intracellular transduction cascades. These cascades control the transcription factors that modulate gene expression, leading to changes in the levels of receptors, ion channels, and other functional proteins. AA, arachidonic acid; ASIC, acid-sensing ion channel; ATP, adenosine triphosphate; CaMKIV, calcium/calmodulin-dependent protein kinase IV; Cox2, cyclooxygenase-2; ERK, extracellular signal-regulated kinase; EP, prostaglandin E receptor; JNK, jun kinase; mRNA, messenger RNA; Na v 1.8/1.9, voltage gated sodium channel type 1.8/1.9; NGF, nerve growth factor; P38, serinethreonine kinase; PKA, protein kinase A; PKC, protein kinase C; TRP, transient receptor potential.
(From Woolf CJ: Pain: Moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004;140:441-451.)

Figure 2–4 Contributions of spinal cord dorsal horn neurons to pain. A. Nociceptive transmission. B. The acute phase of central sensitization. C. The late phase of central sensitization. Some alterations in gene expression are activity-driven and restricted, such as dynorphin, whereas others are widespread and produce diverse changes in function, such as induction of cyclooxygenase-2 (COX-2) in central neurons after peripheral inflammation. D. Disinhibition. AA, arachidonic acid; AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate; EP, prostaglandin E receptor; IL-1, interleukin-1; NK1, neurokinin 1; NMDA, N -methyl-D-aspartic acid; PGE2, prostaglandin E2.
(From Woolf CJ: Pain: Moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004;140:441-451.)

Figure 2–5 Scheme of the Major Signaling Pathways that Regulate TRP Ion Channels. (+) represents sensitization or activation; (−) represents desensitization. In the early phase of inflammation, increased pain sensitivity originates largely as a result of the local release from inflammatory cells of a number of mediators. Most of these inflammatory mediators do not directly activate nociceptors, but rather act as sensitizers, reducing the threshold of the peripheral nociceptor terminals. Among the major inflammatory mediators are prostanoids, particularly prostaglandin E 2 (PGE 2 ), bradykinin, and nerve growth factor. These chemicals acting through EP prostaglandin and B 1 /B 2 bradykinin G protein-coupled receptors and the high-affinity TrkA NGF receptor produce their immediate effects on pain hypersensitivity locally on the nociceptor terminals by phosphorylating TRPV1 as well as the sensory neuron-specific voltage-gated sodium channel Nav 1.8. Activation of the protease-activated receptor 2 by inflammatory proteases like trypsin has a similar effect. Phosphorylation and dephosphorylation substantially alter TRPV1 ion channel function, and this represents a major means of rapidly and dynamically altering pain sensitivity. AA, arachidonic acid; AC, adenylate cyclase; AKAP, A-kinase anchor proteins; B 2 R, bradykinin receptor 2 (BDKRB2); CaM, calmodulin; CaMKII, calmodulin dependent kinase II; COX, cyclooxygenase; DAG, diacylglycerol; EET, epoxyeicosatrienoic acids; EP, prostaglandin E; ER, endoplasmic reticulum; ERK, extracellular-signal-regulated kinases; G11, guanine nucleotide-binding (G) protein-subunits 11; HPETE, hydroperoxyeicosatetraenoic acid; IP 3 R, inositol 1,4,5-trisphosphate receptor; LOX, lipooxygenase; NGF, nerve growth factor; PIP 2 , phosphatidylinositol 4,5-bisphosphate; PIP 3 , phosphatidylinositol (3,4,5)-trisphosphate; PI3K, phosphatidylinositol 3-kinases; PKA, protein kinase A; PKC, protein kinase C; PLA2, phospholipases A2; PLC, phospholipase C; PP2B, protein phosphatase 2B (Calcineurin (CN)); P38, mitogen-activated protein kinases; P450, cytochrome P450; Src, a family of proto-oncogenic tyrosine kinases, Rous sarcoma virus (RSV); Trk A, tyrosine kinase A; TRP, transient receptor potential (has TRPV, TRPM, TRPA, and TRPC subfamilies).
(Modified from Wang H, Woolf CJ. Pain TRPs. Neuron 2005;46:9-12.)

Figure 2–6 Effect of the presence (panel A) and absence (panel B) of downstream regulatory element antagonistic modulator (DREAM) on nociceptive processing after noxious stimulation of the skin with a pin. In panel A, the prodynorphin gene is blocked by DREAM, and the nociceptive signal is transmitted by substance P (SP)-containing dorsal root neurons essentially unaltered through the spinal cord. This activated state is characterized by a large depolarizing potential and multiple spike discharges. Such activity subsequently activates systems governing descending regulatory control and thalamic nuceli, triggering the perception of pain. In panel B, DREAM has been knocked out, and the release of dynorphin from spinal cord interneurons becomes a prominent part of the nociceptive response. This inactivates spinal-projection neurons, leading to a greatly reduced excitatory response. Subsequently, there is almost complete inactivation of descending regulatory and pain-processing systems. In addition to raising issues related to the specific functions of DREAM, this simple scheme emphasizes the importance of neurophysiological research involving this model and hypotheses to guide drug design.
(From Vogt BA. Knocking out the DREAM to study pain. N Engl J Med 2002; 347: 362-364.)
Ectopic excitability, structural reorganization, and decreased inhibition are unique to neuropathic pain, whereas peripheral sensitization occurs in inflammatory pain and in some forms of neuropathic pain.
Pain transient receptor potential (TRP) ion channels are listed in Table 2.2 and illustrated in Figure 2-6 . TRP ion channels are molecular gateways in sensory systems, an interface between the environment and the nervous system. Several TRPs transduce thermal, chemical, and mechanical stimuli into inward currents, an essential first step in eliciting thermal and pain sensations.

Table 2.2 Mammalian Sensory Transient Receptor Potentials (TRPs)

Facet joint pain

Definition
The facet, or zygapophyseal, joint is the set of paired diarthrodial articulations between the posterior elements of the adjacent vertebrae.
Facet joints have been implicated as responsible for spinal pain in 39% of patients with neck pain, 34% of patients with thoracic pain, and 27% of patients with low back pain [1] .

Innervations
The nerve roots are invested by pia mater and covered by arachnoid and dura as far as the spinal nerve. The dura of the dural sac continues around the roots as their dural sleeve, which blends with the epineurium of the spinal nerve ( Fig. 2-7 ).

Figure 2–7 Spinal nerves.
(From Schuenke M, Schulte E, Schumacher U, et al [eds]: Thieme Atlas of Anatomy: General Anatomy and Musculoskeletal System. Stuttgart, Thieme, 2006, p 62.)
Facet joints are well innervated by the medial branches of the dorsal rami, which contain free and encapsulated nerve endings as well as nociceptors and mechanoreceptors. Each segmental medial branch of the dorsal ramus supplies at least two (in humans, monkeys, and cats) or three (in rats) facet joints ( Table 2.3 ).
▪ In the cervical spine below C2-C3, the cervical facet joints are supplied by the medial branches of the cervical rami above and below the joint, which also innervate the deep paramedian muscles.
▪ The C2-C3 joint is supplied by the third occipital nerve.
▪ Innervation of the atlantooccipital and atlantoaxial joints is derived from the C1 and C2 roots, respectively.
▪ In the thoracic and lumbar spine, the facet joints are innervated by medial branches of the dorsal rami of the spinal nerves except at the L5 level.
▪ The L5 dorsal ramus divides into medial and lateral branches, with the medial branch continuing medially, innervating the lumbosacral joint.

Table 2.3 The Lumbar Spinal Nerves
Situations that can lead to pain upon facet joint motion are degeneration, inflammation, and injury of the facet joint.
Pain leads to restriction of motion, which eventually leads to overall physical deconditioning. Irritation of the facet joint innervation in itself also leads to secondary muscle spasm.
The facet has extensive innervation of the synovial lining by small C-type pain fibers, as evidenced by the following findings:
▪ An abundance of protein gene product 9.5 (PGP 9.5)–reactive nerve fibers indicates an extensive innervation of the facet joint capsules.
▪ There are nerve fibers to the facet joint capsules that are reactive to both substance P (SP) and calcitonin gene–related peptide (CGRP) [2] .

Intervertebral disc
The three components of the intervertebral disc (IVD) are as follows:
End plate: This structure consists of a layer of cartilage, resembling articular cartilage that covers the central parts of the inferior and superior cortical bone surfaces of the vertebral bodies.
Nucleus pulposus: The space between the end plates of adjacent vertebrae is filled by the nucleus pulposus (NP), which consists of chondrocytes within a matrix of type II collagen and proteoglycans, mainly aggrecan. The type II collagen fibers are not believed to give the same level of order to the structure or the same degree of mechanical stability to the matrix as in articular cartilage. The proteoglycans are hydrophilic, causing the NP to swell. The swelling pressure of the NP proteoglycans is constrained by the end plates above and below and the anulus fibrosus around the periphery. On tissue sections stained with hematoxylin and eosin, the NP appears homogeneous and pale lilac-blue, consistent with its complement of proteoglycans. In polarized light, it exhibits little birefringence.
Anulus fibrosus: This structure comprises dense sheets of highly ordered collagen fibers (mainly type I but also types II and III) in which are cells with the morphology and phenotype of fibroblasts. Functionally, the anulus fibrosus (AF) is a very strong ligament binding together the outer rims of adjacent vertebrae. On tissue sections stained with hematoxylin and eosin, the AF exhibits fairly uniform eosinophilia, and in polarized light, its constituent alternating bands of highly orientated collagen fibers are clearly seen.

Distinguishing “Normal Aging” from Disease of the Intervertebral Disc
Figures 2-8 and 2-9 and Table 2.4 contain information pertinent to this issue.

Figure 2–8 Questionable radiographic diagnoses that increase in frequency with age, from imaging studies of patients without symptoms. CT, computed tomography; DJD, degenerative joint disease; MRI, magnetic resonance imaging.
(From Loeser JD: Low back pain. In Loeser JD, Butler SH, Chapman CR, Turk DC [eds]: Bonica’s Management of Pain, 3rd ed. Philadelphia, Lippincott Williams & Wilkins, 2001, p 1520.)

Figure 2–9 Forces within the nucleus pulposus and annulus of a nondegenerated disc ( left ) and degenerated disc ( right ) under compression.
(From Urban JPG, Roberts S: The intervertebral disc: Normal, aging, and pathologic. In Herkowitz HN, Garfin SR, Eismont FJ, et al [eds]: Rothman-Simeone The Spine, 5th ed. Philadelphia, Saunders, 2006, p 133.)
Table 2.4 Pathophysiology of Intervertebral Disc Aging and Degeneration Process Effects Diminished cellular response Senescence (alteration in gene expression and transcription factors)   Apoptosis (programmed cell death) Biochemical processes Imbalance between catabolic and anabolic activity:
Post-translational protein modification
Increased collagen cross-linking through nonenzymatic glycation, lipid peroxidation
Loss of proteoglycans
Altered diffusion of nutrients
Impaired assembly of newly synthesized molecules End plate changes Diminished vascularity and decreased porosity because of end plate calcification → elevated lactate concentrations and reduced pH → cell apoptosis   Thinning or microfracture of the end plate → increased permeability and altered hydraulic property → nonuniform load transference and increased focal shear stress → disc degeneration and anular damage
From Biyani A, Andersson GBJ: Low back pain: Pathophysiology and management. J Am Acad Orthop Surg 2004;12:106-115.

Altered Matrix Composition and Integrity
Normal discal chondrocytes are characterized by expression of type II collagen and proteoglycans and are regulated by the “master chondroregulatory gene,” SOX-9. In cases of disc degeneration, increased synthesis of collagens I and III and decreased production of aggrecan are noted. Furthermore, the regulation of matrix turnover is deranged, affecting both synthesis and degradation. There is a net increase in matrix-degrading enzyme activity over natural inhibitors of such activity, which leads to loss of discal matrix. Particular attention has been paid to the role of matrix metalloproteinases (MMPs) in these processes, making them a potential target for therapy designed to inhibit disc degeneration.
After work on the mechanism of aggrecan degradation in articular cartilage, interest has now grown in the possible role of aggrecanases in IVD degeneration. Aggrecan has two cleavage sites, one acted upon by MMPs and the other by members of a group of enzymes called the ADAMs family (after their hybrid function, a disintegrin and metalloproteinase). In fact, the aggrecanases are two enzymes, ADAMTS4 and ADAMTS5, that in addition to their disintegrin and metalloproteinase function also have thrombospondin motifs (hence the TS). From the pathologic perspective, these studies have largely been undertaken, not by looking for the enzymes themselves, but through the application of antibodies targeted at the breakdown product of aggrecan formed by enzyme action at the specific site.

Reduced Cell Number
The reduction in chondrocytes that typifies IVD degeneration has been ascribed to apoptosis. There is some evidence of a “dose-dependent” relationship between apoptosis and excessive load (lifestyle, body weight, age). As in other chondroid tissues, nitric oxide has been implicated in the induction of apoptosis in the IVD.

Nerve and Blood Vessel Ingrowth
Although the normal adult IVD is avascular and aneural, nerves and blood vessels grow into diseased IVD. One avenue of investigation has been the local production of angiogenic and neurogenic molecules within degenerate IVD ( Fig. 2-10 ), which has yielded the following findings:
▪ Expression of the potent angiogenic factor vascular endothelial growth factor (VEGF) has been demonstrated within the IVD.
▪ An investigation of the active (β) chain of nerve growth factor (NGF) expression by cells in the IVD has shown that NGF is synthesized by blood vessels in discs showing nerve ingrowth. Furthermore, the small nerves adjacent to the vessels express the high-affinity receptor for NGF, TrkA (tyrosine kinase A) [3] .

Figure 2–10 Schematic view of the routes for nutrient transport into the avascular disc and resulting nutrient profiles.
(Reprinted from Urban JPG, Roberts S: The intervertebral disc: Normal, aging, and pathologic. In Herkowitz HN, Garfin SR, Eismont FJ, et al [eds]: Rothman-Simeone The Spine, 5th ed. Philadelphia, Saunders, 2006, p 77.)
The implication of these findings is that although either angiogenesis or neuronogenesis could be targets for therapy, angiogenesis drives nerve ingrowth and may be more significant from a therapeutic perspective.

Cytokines as regulators of disease processes
There has also been growing interest in the possible role of cytokines in regulating the connective tissue degradation, nerve and vessel ingrowth, and macrophage accumulation that characterize IVD degeneration ( Table 2.5 ) [4, 5] . A number of cytokines have been implicated, including TNF (tumor necrosis factor) ( Fig. 2-11 ), IL-1 (interleukin-1), IL-6, and IL-10, PDGF (platelet-derived growth factor), VEGF (vascular endothelial growth factor), IGF-1 (insulin-like growth factor-1), TGF-β (transforming growth factor-β), EGF (epidermal growth factor), and FGF (fibroblast growth factor) [6] .
Table 2.5 Common Chemical Substances and Their Functions Chemical Substance Function Phospholipase A 2 Mediates mechanical hyperalgesia Nitric oxide Inhibits mechanical hyperalgesia and produces thermal hyperalgesia MMP-2 (gelatinase A) and MMP-9 (gelatinase)
Degrade gelatin (denatured fibrillar collagens) and other matrix molecules
Act synergistically with MMP-1 MMP-1 (collagenase-1) Degrades collagen MMP-3 (stromelysin-1) Both MMP-1 and MMP-2 may play a role in spontaneous regression of the herniated disc IL-1, TNF-α, prostaglandin E 2
Promote matrix degradation
Enhance production of MMPs Calcitonin gene–related peptide, glutamate, substance P (neurotransmitters) Modulate dorsal root ganglion responses IL-6 Induces synthesis of TIMP-1 TIMP-1 Inhibits MMPs Transforming growth factor-β superfamily Blocks synthesis of MMPs Insulin-like growth factor-1, platelet-derived growth factor Have an anti-apoptotic effect
IL, interleukin; MMP, matrix metalloproteinase; TIMP, tissue inhibitor of metalloproteinase.
From Biyani A, Andersson GBJ: Low back pain: Pathophysiology and management. J Am Acad Orthop Surg 2004;12:106-115.

Figure 2–11 Suggested mechanism of action for tumor necrosis factors (TNF). A, TNF from cells of the herniated nucleus pulposus enters endothelial adhesion molecules such as intracellular and vascular cellular adhesion molecules (ICAM and VCAM). B, Circulating white blood cells adhere to the vessel walls (1) and extravasate from the capillaries out among the axons due to a TNF-induced increase in vascular permeability (2). TNF also induces an accumulation of thrombocytes that will form an intravascular thrombus (3). C, There is a local release of TNF from the extravasated white blood cells among the axons that will induce myelin injury, an accumulation of sodium channels, and allodynic events in the dorsal root ganglion (DRG) and at the spinal cord level. The thrombus, together the edema due to the increased permeability, will induce a nutritional deficit in the nerve root. Both the local effects of TNF and the nutritional deficit may induce pain and nerve dysfunction.
(From Olmarker K, Myers R, Kikuchi S, Meyers RR: Sciatica and nerve root pain in disc herniation and spinal stenosis: a basic science review and clinical perspective. In Herkowitz HN, Gardin SR, Eismont FJ, Bell GR, Balderston RA [eds]. Rothman-Simeone The Spine, 5th ed. Philadelphia, Saunders, 2006, p 101.)
Studies of IL-1 have yielded the following findings:
▪ IL-1 has a role in maintaining cartilage homeostasis, largely through its ability to switch chondrocytes from anabolism to catabolism, inducing cartilage breakdown at molecular and morphologic levels.
▪ It is a regulator of angiogenesis in joints and nonarticular cartilage, possibly by acting as a promoter of the potent angiogenic factor VEGF.
▪ In the IVD, both of the isoforms, IL-1α and IL-1β, have been shown to increase proteoglycan release and degradative enzyme production.
▪ IL-1α and IL-1β have also been found to increase the production of MMPs and pain mediators, such as the eicosanoid prostaglandin E 2 , by human IVD cells.
▪ IL-1 can mediate some of the other characteristics of IVD disease, such as nerve and vessel ingrowth.
As IL-1 is the regulator of cartilage catabolism, the TGF-β superfamily is the regulator of cartilage anabolism. A twofold increase was seen in proteoglycan synthesis by rabbit nucleus pulposus cells after injection of rabbit intervertebral discs with an adenoviral vector carrying a human TGF-β transgene [6] .

Nomenclature and classification of lumbar disc pathology
The North American Spine Society (NASS), the American Society of Spine Radiology (ASSR), and the American Society of Neuroradiology (ASNR) have determined nomenclature for and classification of lumbar disc pathology, which are summarized here.
General classifications of disc lesions are listed in Box 2.3 and described here:
Normal disc: A disc is considered normal if it is young and morphologically normal, without consideration of the clinical context. This would not include degenerative, developmental, or adaptive changes that could, in some contexts (e.g., normal aging, scoliosis, and spondylolisthesis) be considered clinically normal. However, the bilocular appearance of the adult nucleus resulting from the development of a central horizontal band of fibrous tissue is considered a sign of normal maturation. The disc space is defined craniad and caudad by the vertebral body end plates and peripherally by the outer edges of the vertebral ring apophyses, exclusive of osteophytic formations.
Congenital/developmental variant: This category includes discs that are congenitally abnormal or that have undergone changes in their morphology as an adaptation to abnormal growth of the spine, such as from scoliosis or spondylolisthesis.
Degenerative/traumatic: The use of the terms degenerative and traumatic to describe this group does not imply that trauma is necessarily a factor or that degenerative changes are necessarily pathologic. These changes may be a result of the normal aging process.
Anular tears: Also properly called “anular fissures,” anular tears are separations between anular fibers, avulsion of fibers from their vertebral body insertions, or breaks through fibers that extend radially, transversely, or concentrically, involving one or many layers of the anular lamellae. “Tear” and “fissure” describe the spectrum of such lesions and do not imply that the lesion is consequent to trauma ( Fig. 2-12 ).
Degeneration: Disc degeneration may involve any or all real or apparent desiccation, fibrosis, narrowing of the disc space, diffuse bulging of the anulus beyond the disc space, extensive fissuring (i.e., numerous anular tears), and mucinous degeneration of the anulus, defects and sclerosis of the end plates, and osteophytes at the vertebral apophyses. A disc demonstrating one or more of these degenerative changes can be further qualified into one of two subcategories, spondylosis deformans —possibly representing changes in the disc associated with a normal aging process—and intervertebral osteochondrosis —possibly the consequence of a more clearly pathologic process ( Fig. 2-13 ).
Herniation: Herniation is defined as a localized displacement of disc material beyond the limits of the intervertebral disc space ( Fig. 2-14 ). Disc material may be nucleus, cartilage, fragmented apophyseal bone, anular tissue, or any combination thereof.

BOX 2.3 General Classification of Disc Lesions*
Modified from Milette PC: Classification, diagnostic imaging, and imaging characterization of a lumbar herniated disc. Radiol Clin North AM 2000;38:1267-1292.

1. Normal (excluding aging changes)
2. Congenital/developmental variant
3. Degenerative/traumatic lesion:
1) Anular tear (Anular fissure)
2) Herniation:
(1) Protrusion/extrusion
(2) Intervertebral
3) Degeneration:
(1) Spondylosis deformans
(2) Intervertebral osteochondrosis
4. Inflammation/infection
5. Neoplasia
6. Morphologic variant of unknown significance

Figure 2–12 Schematic sagittal anatomic sections showing the differentiating features of a normal disc, an anular tear (radial tear in this case), and a disc herniation. The term tear is used to refer to a localized radial, concentric, or horizontal disruption of the anulus without associated displacement of disc material beyond the limits of the intervertebral disc space. Nuclear material is shown in red, and the anulus (internal and external) corresponds to the gray portion of the intervertebral space.
(From Milette PC: Classification, diagnostic imaging and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000;38:1267-1292.)

Figure 2–13 Schematic sagittal anatomic sections showing the differentiating characteristics of a normal disc, spondylosis deformans, and intervertebral osteochondrosis. The distinction between these three entities is usually possible on all imaging modalities, including conventional radiographs.
(From Milette PC: Classification, diagnostic imaging and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000;38:1267-1292.)

Figure 2–14 Herniated disc refers to localized displacement of nucleus, cartilage, fragmented apophyseal bone, or fragmented anular tissue beyond the intervertebral disc space (disc space, interspace). The interspace is defined, craniad and caudad, by the vertebral body end plates. Two intravertebral herniations, one with an upward orientation and the other with a downward orientation with respect to the disc space, are illustrated schematically.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

Classifications of Disc Herniation
Figure 2-15 illustrates, and Box 2.4 summarizes, the proposed categories for the description and classification of disc herniation, which are as follows [7] :
▪ Generalized disc herniation: defined as greater than 50% (180 degrees) of the periphery of the disc.
▪ Localized displacement in the axial (horizontal) plane, which is further classified as focal (involving less than 25% of the disc circumference) or broad-based (involving between 25% and 50% of the disc circumference.

Figure 2–15 The interspace is defined, peripherally, by the edges of the vertebral ring apophyses, exclusive of osteophytic formations. A, The line drawing schematically illustrates a localized extension of disc material beyond the intervertebral disc space, in a left posterior direction, which qualifies as a disc herniation. B, For classification purposes, the intervertebral disc is considered a two-dimensional round or oval structure having four 90-degree quadrants. By convention, a herniation is a localized process involving less than 50% (180 degrees) of the disc circumference. C, By convention, a focal herniation involves less than 25% (90 degrees) of the disc circumference. D, By convention, a broad-based herniation involves between 25% and 50% (90 to 180 degrees) of the disc circumference. E, Symmetrical presence (or apparent presence) of disc tissue circumferentially (50%-100%) beyond the edges of the ring apophyses may be described as a “bulging disc” or “bulging appearance” and is not considered a form of herniation. Furthermore, bulging is a descriptive term for the shape of the disc contour and not a diagnostic category. F, Asymmetrical bulging of the disc margin (50%-100%), such as found in severe scoliosis, is also not considered a form of herniation. Herniated discs may take the form of protrusion ( G ) or extrusion ( H ), according to the shape of the displaced material.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

BOX 2.4 Proposed Categories for Description and Classification of a Disc Herniation
Modified from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2003;26:E93-E113.

1. Morphology:
1) Protrusion
2) Extrusion
3) Intravertebral
2. Containment
3. Continuity
4. Relation with posterior longitudinal ligament complex
5. Volume
6. Composition
7. Location
Bulging disc, which is defined as the presence of disc tissue “circumferentially” (50%-100%) beyond the edges of the ring, is not considered a form of herniation, nor are diffuse adaptive alterations of disc contour secondary to an adjacent deformity as may be present in severe scoliosis or spondylolisthesis.
The distinction between protrusion and extrusion of a disc herniation is clarified by Figures 2-16 and 2-17 .

Figure 2–16 When a relatively large amount of disc material is displaced, distinction between protrusion ( A ) and extrusion ( B or C ) generally possible only on sagittal magnetic resonance images or sagittal computed tomography (CT) reconstructions. C, Although the shape of the displaced material is similar to that of a protrusion, the greatest craniocaudal diameter of the fragment is greater than the craniocaudal diameter of its base at the level of the parent disc, and the lesion therefore qualifies as an extrusion. In any situation, the distance between the edges of the base, which serves as reference for the definition of protrusion and extrusion, may differ from the distance between the edges of the aperture of the anulus, which cannot be assessed on CT scans and is seldom appreciated on MR images. In the craniocaudal direction, the length of the base cannot exceed, by definition, the height of the intervertebral space.
(From Milette PC: Classification, diagnostic imaging and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000;38:1267-1292.)

Figure 2–17 Schematic representation of various types of posterior central herniations. A, Small subligamentous herniation (or protrusion) without significant disc material migration. B, Subligamentous herniation with downward migration of disc material under the posterior longitudinal ligament (PLL). C, Subligamentous herniation with downward migration of disc material and sequestered fragment.
(From Milette PC: Classification, diagnostic imaging and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000;38:1267-1292.)
Complications of herniated discs are illustrated in Figure 2-18 .

Figure 2–18 Relationship of typical posterior disc herniations with the posterior longitudinal ligament (PLL). A, Midline sagittal section. Unless very large, a posterior midline herniation usually remains entrapped underneath the deep layer of the PLL, and sometimes a few intact outer anulus fibers join with the PLL to form a “capsule.” The deep layer of the PLL ( arrow ) also attaches to the posterior aspect of the vertebral body so that no potential space is present underneath. B, Sagittal paracentral section. The PLL extends laterally at the disc level ( arrow ) but above and below the disc, an anterior epidural space (as), where disc fragments are frequently entrapped, is present between the lateral (peridural) membranes and the posterior aspect of the vertebral bodies.
(From Milette PC: Classification, diagnostic imaging and imaging characterization of a lumbar herniated disc. Radiol Clin North Am 2000;38:1267-1292.)
Figures 2-19 through 2-22 summarize the nomenclature for the anatomic zones and levels of the spine.

Figure 2–19 Coronal drawing illustrating the main anatomic zones and levels of a spinal segment.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

Figure 2–20 Schematic representation of the anatomic zones of the vertebral body identified on axial images. The anterior zone ( not shown ) is delineated from the extraforaminal zone by an imaginary coronal line in the center of the vertebral body.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

Figure 2–21 Schematic representation of the anatomic levels of a spinal segment identified on craniocaudal images.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

Figure 2–22 Schematic summative representation of anatomic levels and zones of a spinal segment.
(Adapted from Fardon DF, Milette PC; Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology: Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine 2001;26:E93-E113.)

Dorsal root ganglion
Edema in the dorsal root ganglion is the basis of the production of nerve root pain in patients with disc herniation. Mechanosensitivity and chemosensitivity of the dorsal root ganglion have been demonstrated. Experimentally applied nucleus pulposus from both healthy and degenerative discs reduces nerve root conduction velocity, suggesting a pathomechanism of neural injury. The pertinent findings are as follows:
▪ The nucleus pulposus can induce excitatory changes, rising endoneurial pressures, and compartment syndrome, and can cause intraneural thrombi in the DRG or the nerve roots.
▪ Anti-inflammatory agents, such as tumor-necrosis factor-α (TNF-α) inhibitors, may protect against nucleus pulposus–induced injury to the DRG and nerve roots.

Sacroiliac joint
The pain sensitivity of the sacroiliac joints may be lower than that of lumbar facet joints but higher than that of the anterior portions of the lumbar discs. A high prevalence of sacroiliac joint pain may be seen in patients with post–lumbar fusion pain.

Postlaminectomy syndrome
Animal models of postlaminectomy syndrome demonstrate paraspinous muscle spasms, tail contractures, behavioral pain behaviors, tactile allodynia, epidural and perineural scarring, and adherence of the nerve root to the underlying disc and pedicle.
Suggested causes of postlaminectomy syndrome include acquired stenosis, adjacent segment degeneration, internal disc disruption, recurrent disc herniation, retained disc fragment, spondylolisthesis, epidural or intraneural fibrosis, degenerative disc disease, radiculopathy, radicular pain, deconditioning, facet joint pain, sacroiliac joint pain, discitis, arachnoiditis, pseudoarthrosis, and segmental instability. Among these, etiologies such as epidural fibrosis, facet joint dysfunction, sacroiliac dysfunction, internal disc dysfunction, recurrent disc herniation, and spinal stenosis can be treated by interventional pain techniques. Ultimately, many of these causes are interrelated.
Facet joint involvement in chronic pain following lumbar surgery has been shown to be present in approximately 8% to 16% of patients. Through the use of a single nerve block, one study found the prevalence of sacroiliac joint pain following lumbar fusion to be 35% [8] .
Epidural fibrosis may occur after an annular tear, disc herniation, hematoma, infection, surgical trauma, vascular abnormalities, or intrathecal injection of contrast media. Epidural fibrosis may account for as much as 20% to 36% of all cases of failed back surgery syndrome. Alternatively, there may be a final common pathway for all these etiologies that results in peripheral and central facilitation potentiated by inflammatory and nerve injury mechanisms. Paraspinal muscles may also become denervated and involved in the pathogenesis of failed back surgery syndrome [8] .

Spinal stenosis
Spinal stenosis can be defined as a narrowing of the spinal canal that results in symptoms and signs due to entrapment and compression of the intraspinal vascular and nervous structures. Disc bulging, protrusion, and herniation in the cervical as well as lumbar areas, combined with osteophytes and arthritic changes of the facet joints, can cause narrowing of the spinal canal, encroachment on the contents of the dural sac, or localized nerve root canal stenosis ( Fig. 2-23 ).

Figure 2–23 Algorithm describing pathogenesis of lumbar stenosis. DDD, Degenerative Disc Disease.
(Adapted from Akuthota V, Lento P, Sowa G: Pathogenesis of lumbar spinal stenosis pain: Why does an asymptomatic stenotic patient flare? Phys Med Rehabil Clin North Am 2003;14:17-28.)

References

1 Manchukonda R., Manchikanti K.N., Cash K.A., et al. Facet joint pain in chronic spinal pain: An evaluation of prevalence and false-positive rate of diagnostic blocks. J Spinal Disord Tech . 2007;20:539-545.
2 Kallakuri S., Singh A., Chen C., Cavanaugh J.M. Demonstration of substance P, calcitonin gene-related peptide, and protein gene product 9.5 containing nerve fibers in human cervical facet joint capsules. Spine . 2004;29:1182-1186.
3 Freemont A.J., Watkins A., Le Maitre C., et al. Nerve growth factor expression and innervation of the painful intervertebral disc. J Pathol . 2002;197:282-286.
4 Biyani A., Andersson G.B.J. Low back pain: Pathophysiology and management. J Am Acad Orthop Surg . 2004;12:106-115.
5 Freemont A.J., Watkins A., Le Maitre C., et al. Current understanding of cellular and molecular events in intervertebral disc degeneration: Implications for therapy. J Pathol . 2002;196:374-379.
6 Nishida K., Kang J.D., Gilbertson L.G., et al. Modulation of the biologic activity of the rabbit intervertebral disc by gene therapy: An in vivo study of adenovirus-mediated transfer of the human transforming growth factor beta 1 encoding gene. Spine . 1999;24:2419-2425.
7 Fardon D.F., Milette P.C., Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Nomenclature and classification of lumbar disc pathology: Recommendations of the Combined Task Forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine . 2003;26:E93-E113.
8 Boswell M.V., Shah R.V., Everett C.R., et al. Interventional techniques in the management of chronic spinal pain: Evidence-based practice guidelines. Pain Physician . 2005;8:1-47.
Chapter 3 Radiologic Anatomy of the Spine

Hak-Jin Kim, MD, PhD

The cervical spine
The first two cervical vertebrae, the atlas and the axis, and the last cervical vertebra are structurally special. However, the C3 to C6 vertebrae are fairly uniform and can be described together. The atlas and axis form a complex articular system for both the nodding and rotational movements of the head. These bony structures of the base of the skull and the craniocervical junction are better seen on computed tomography (CT) than on magnetic resonance imaging (MRI). The atlas and the axis are linked together and to the skull and other cervical vertebrae by several ligaments.

Atlas (C1)
The atlas supports the weight of the skull and is very appropriately named after the mythical giant who carried the earth on his shoulders. It is a bony ring consisting of an anterior arch and a posterior arch , which are connected by two lateral masses . The anterior arch forms a short bridge between the anterior aspects of the lateral masses. On the posterior surface of the anterior arch, a midline facet marks the synovial articulation of the odontoid process of the axis, and internal tubercles on the adjacent lateral masses show the attachments of the transverse atlantal ligaments that hold the odontoid against this articular area. The posterior arch consists of modified laminae that are round and a posterior tubercle that represents a rudimentary spinous process. The atlas is devoid of a body and of a full spinous process .
The lateral masses consist of superior and inferior articular facets and transverse processes . The superior articular facets are concave and ovoid, and they face upward and inward as shallow foveae for articulation with the occipital condyles. Nutatory movements of the head mainly occur at these atlantooccipital joints. The inferior articular facets are concave and face downward, slightly medially, and backward; they articulate with the superior articular facets of the axis. The relative horizontal orientation of the atlantoaxial facet joints allows rotation at the expense of bony stability. The paired alar ligaments, running from the posterolateral aspects of the odontoid process to the occipital condyles, prevent excessive rotation [1] . The transverse processes are each pierced by a foramen for the vertebral artery. On coronal CT scans, the occipitoatlas and the atlantoaxial joints resemble a capital X.

Axis (C2)
The second cervical vertebra, or axis, supports the dens, or odontoid process, which projects rostrally from the body, serving as a pivotal restraint against horizontal displacement of the atlas. Unlike the remaining portions of the cervical spine, on MRI the dens can demonstrate a decreased signal relative to other vertebral bodies, presumably because of partial volume averaging. Embryologically, the odontoid process fuses with the body by 3 to 6 years of age. A persistent remnant of the subdental synchondrosis is often recognized on sagittal MR images or on reformatted sagittal CT scans as a horizontal dark band at the base of the odontoid process; this is a normal feature and should not be mistaken for a fracture.
The space between the clivus, the anterior arch of the atlas, and the tip of the odontoid process demonstrates high signal intensity on MRI owing to its fat component. Also, the fatty marrow of the clivus, the occipital condyle, and the arch of C1 appear as high signal intensities on a T1-weighted MR image. The cortical bone and the articular surface show low signal intensity, and the vertebral artery exhibits its characteristic signal void. The inferior articulating surfaces of the axis begin the typical articular columns of the cervical vertebrae. The lateral processes of the axis are directed downward, and their posterior or noncostal elements are often quite thin. Anteriorly, the inferior aspect of the body of the axis forms a liplike process that descends over the first intervertebral disc and the body of the third cervical vertebra.

The Ligaments of the Atlas and Axis
The axis and atlas are anchored to the skull base by several layers of strong ligaments, the apical and lateral alar ligaments. These ligaments are covered by the broad tectorial membrane, an anterior layer of the posterior longitudinal ligament. Posteriorly, the occiput and the atlas are connected by the thin, wide, elastic posterior atlantooccipital membrane , which is pierced by the vertebral artery and the first cervical nerve. Anteriorly, the broad atlantooccipital and atlantoepistrophic ligaments are partially hidden by the anterior longitudinal ligament . The alar ligaments and the longitudinal bundles of the cruciate ligament of the atlas are not discernible from the cortical bone on MRI. On T1-weighted MR images, the transverse ligament is represented by a band of low signal intensity that joins the medial aspect of the lateral masses of the atlas.

C3 to C7 Vertebrae

Vertebral Bodies
The vertebral bodies in the cervical spine are ladder-like in cross section; they are broader in the transverse diameter than in the anteroposterior (AP) dimension, and their end plates are parallel ( Fig. 3-1 ). The cervical vertebral bodies are smaller than those of the other movable vertebrae and increase in size from C3 downward. The vertebrae are connected by the anterior and posterior longitudinal ligaments . Each ligament’s fibers diverge at each disc level and blend with the anulus fibrosus and the adjacent margins of the vertebral bodies. At the mid-vertebral level, the posterior longitudinal ligament is narrower and lies behind the body, posterior to the retrovertebral venous plexus.

Figure 3–1 T1-weighted coronal MR image shows the outline of the cervical spine. The cervical vertebral bodies are stepladder-like in this view. The bodies are broader in the transverse diameter than superoinferior dimension.

Joints of von Luschka
The upper and lateral edges of the superior surface project upward and have sagittal ridges that form the uncinate processes. Together with corresponding notches in lower end plates of the vertebra above, they form the uncovertebral joints of von Luschka ( Fig. 3-2 ).

Figure 3–2 T2-weighted coronal MR image presents the uncovertebral joints of von Luschka ( large arrows ). The uncinate process from the upper lateral edge of the superior surface of the lower vertebral body faces the lower lateral notch in the lower end plate of upper vertebral body. Small arrows indicate the vertebral arteries.

Transverse Foramen
The transverse foramen, a characteristic feature of the cervical spine, houses the vertebral artery, veins, and sympathetic nerves in the deep cranial groove of the transverse process. The spinal nerves and ganglia cross the dorsal border of the artery along with segmental vessels. The transverse foramen of the seventh cervical vertebra contains only vertebral veins, not the vertebral artery ( Figs. 3-3 and 3-4 ).

Figure 3–3 Axial CT scan of the seventh cervical vertebra. The transverse foramen of the seventh cervical vertebra contains only vertebral veins ( thin arrow ), not the vertebral artery ( thick arrows ). However, the other cervical vertebrae contain the vertebral artery within their transverse foramina. See also Fig. 3-4 .

Figure 3–4 T1-weighted axial MR image corresponding to the CT scan in Fig. 3-3 . The vertebral arteries are revealed as signal voids ( arrows ) anterior to the transverse foramina.

Pedicles
The pedicles are short, cylindrical structures. They project posterolaterally from the bodies and are grooved by superior and inferior vertebral notches, of almost equal depth, that form the intervertebral foramina. Axial sections through the pedicles reveal that the spinal canal is completely surrounded by bone.

Laminae
The laminae are two V-shaped supports of bone emerging from the pedicles. They join at the midline to form the spinous process, and they bear the bifid spinous process at the postero-midline junction that receives the insertions of the semispinalis cervicis muscles.

Articular Processes
The superior and inferior articular processes of adjacent neural arches form the facet joints. These structures are more oblique in the cervical level than in other levels of the spine. Each joint surface is lined with articular cartilage, and menisci cushion the cervical facets. Surrounding each joint is a fibrous capsule with a synovial membrane on its inner aspect; this capsule is relaxed to allow a gliding motion. Anteriorly, the superior articular facet is rounded in its anterior aspect; its articular surface faces posteriorly and is flat. Posteriorly, the inferior articular facet of the vertebra above has a flat anterior articular surface and a convex posterior aspect ( Fig. 3-5 ).

Figure 3–5 The superior articular process of the lower vertebral body, located at the anterior aspect of the facet joint, is shown facing posteriorly, and its flat articular surface can be seen. The inferior articular process of the vertebra has a flat anterior articular surface and a convex posterior aspect.

Spinal Canals
The spinal canals are relatively large in order to house the cervical enlargement of the spinal cord. The spinal canal is triangular with the apex of the triangle posterior. The canal decreases in size from vertebra C1 through vertebra C3 and has a fairly uniform dimension from C3 through C7. C7 is a transitional vertebra, whose spinous process is longer and thicker and has a more inferior tilt than the more rostral cervical spinous processes of C3 to C6. On a T1-weighted MR image, the exact size of the subarachnoid space is difficult to assess because of its low signal intensity, and it may be confused with the posterior longitudinal ligament and the cortical bone ( Fig. 3-6 ).

Figure 3–6 The subarachnoid space, the posterior longitudinal ligament, and the cortical bone reveal low signal intensity on this T1-weighted MR image. They cannot be defined individually.

Epidural Space
The epidural space that surrounds the dural sac contains neurovascular and connective tissue elements that are more clearly seen on MRI and CT after intravenous injection of a contrast agent. There is only a small amount of epidural fat tissue , and sinuses are formed in this fat tissue by the wide venous plexuses that surround roots and nerves as they leave the intervertebral foramina in the lateral parts of the epidural space ( Fig. 3-7 ). The scarcity of revised epidural fat in the cervical canal in comparison with that in the lumbar canal makes it more difficult to differentiate between the soft tissue structures in the cervical spinal canal on a noncontrast CT scan. On MRI, the high signal intensity in the anterior lateral aspect of the cervical canal represents the epidural venous plexus . The epidural venous plexuses produce high signal intensity in the anterior epidural space, which should not be confused with epidural fat; epidural fat is virtually absent at the cervical level.

Figure 3–7 There is little epidural fat tissue in the cervical spine. Wide venous plexuses surround roots and nerves in the lateral aspect of the epidural space and the vertebral artery within the transverse foramen on this contrast-enhanced axial CT scan.

Cervical Discs
The cervical intervertebral discs are smaller than the discs of other regions of the spine. The uncinate processes on the upper end plate limit lateral extension of the discs. These discs are wedge-shaped, the greater width being anterior, corresponding to the cervical lordosis [2] . The intervertebral discs do not extend anteriorly or posteriorly beyond the level of the vertebral body in younger people. The nucleus pulposus cannot be differentiated from the anulus fibrosus, but the periphery of the disc is less intense than its central portion. ( Figs. 3-6 and 3-8 ).

Figure 3–8 On T2-weighted sagittal MR images, high signal intensity can be seen in the nucleus pulposus and the anulus pulposus, which thus cannot be differentiated. The periphery of the disc shows a slightly lower signal intensity than the center.

Nerves of the Cervical Cord
Spinal nerves arise from the cervical cord. Each nerve consists of a dorsal sensory root and a ventral motor root. The nerve roots join just lateral to the dural sheath to form the spinal nerves. The dorsal root ganglion is located in the neural foramen just proximal to the point of union of the dorsal and ventral roots. The roots of each spinal nerve from C1 through C7 leave the spinal canal through the intervertebral foramina above the corresponding vertebra. The eighth cervical nerve passes through the foramen between C7 and T1. The spinal ganglion, located outside and below the neural foramen, is clearly seen posterior to the vertebral artery on MRI as a structure of intermediate signal intensity. On contrast-enhanced MR images, the spinal ganglion appears as a mildly enhancing ovoid structure posterior to the vertebral artery ( Fig. 3-9 ).

Figure 3–9 On a contrast-enhanced T1-weighted axial MR image, the spinal ganglion shows intermediate signal intensity posterior to the vertebral artery ( arrows ).

Vertebral Arteries
The vertebral arteries usually enter the foramina at the C6 level but may enter at C5 or C7, and they exit the foramina in the area of the transverse process of the atlas; they wind around the lateral masses, passing in a group just posterior to the superior articular facet, from the cranial surface to the posterior arch [3] . The two vertebral arteries penetrate the dura and are well demonstrated on each side of the medulla on contrast-enhanced CT. Within the transverse foramen ( Fig. 3-10 ), the vertebral artery is of low signal intensity ( Fig. 3-11 ), and the vertebral vein of high signal intensity, on MRI. The vertebral vein surrounds the vertebral artery.

Figure 3–10 The vertebral artery ( arrow ) exits the transverse foramen of the atlas, curves posterolaterally, penetrates the dura, and enters the spinal canal, as seen on this contrast-enhanced axial CT scan.

Figure 3–11 The common carotid arteries, the internal jugular veins, and the vertebral arteries have low signal intensity on this T2-weighted axial MR image. Sometimes, slow-flowing veins have intermediate to high signal intensity on MRI.

Venous Plexus
The cervical epidural venous plexus is an extensive sinusoidal network in the cervical epidural space; it consists of medial and lateral longitudinal channels in the anterolateral portion of the epidural space. The medial and lateral longitudinal channels are connected behind each vertebral body by retrocorporeal veins that communicate with the basivertebral venous system at the midportion of each vertebral body, as follows ( Fig. 3-12 ):
▪ The anterior internal veins , which lie behind the vertebral bodies, receive veins from the ventral dura and vertebral bodies.
▪ The posterior internal veins , which lie ventral to the vertebral arches and ligamenta flava receive veins from these structures.
▪ The external venous plexus lies outside the vertebral channel, along the surfaces of the vertebral bodies, and communicates with the internal plexus through veins in the neural foramina.
▪ The longitudinal channels communicate with the foraminal venous plexus , which extends anteriorly to surround the vertebral artery on each side.

Figure 3–12 Contrast-enhanced MR venography shows an extensive sinusoidal network in the cervical epidural space. Each level of the cervical spine reveals the basivertebral vein (BV) communicating with the anterior longitudinal epidural veins (ALV) via the retrocorporeal veins (RV). The venous plexus (VP) surrounding the vertebral artery connects the longitudinal veins via the communicating veins (CV).
This system is an intricate, lattice-like network composed of slowly flowing blood [3] . The veins can be seen on both sagittal and axial MR images as areas of increased signal intensity. Parasagittal views demonstrate them best in the anterolateral recess of the cervical spinal canal. Increased intensity denotes slow to stagnant venous flow. Axial images show these segmented longitudinal bandlike channels as areas of high signal intensity in the anterolateral recess of the spinal canal. Though often seen on noncontrast studies, the epidural venous plexus can be unclear, depending on the direction and velocity of blood flow. It is more consistently and accurately depicted after the administration of gadolinium-DTPA , which produces a uniformly high signal intensity of the epidural venous structures outside the extradural space, along the anterolateral aspects of the spinal canal and neural foramina.

The thoracic spine
The 12 thoracic vertebrae are intermediate in size between the smaller cervical and larger lumbar vertebrae. The vertebral bodies and their discs have an inverted heart shape in cross section. The end plates of the vertebral bodies are flat, and the nuclei pulposi are more centrally located than in the lumbar discs. The thickness and the horizontal dimensions of the thoracic discs increase caudally. Although the thoracic discs are of larger volume than the cervical discs, they are thinner vertically than cervical and lumbar discs ( Fig. 3-13 ). The thoracic vertebrae are characterized by costal facets on both sides of the bodies and on all the transverse processes except those of the 11th and 12th thoracic vertebrae, which articulate with facets on the heads and tubercles, respectively, of the corresponding ribs ( Fig. 3-14 ).

Figure 3–13 T2-weighted sagittal MR image. Thoracic vertebral bodies and discs increase in transverse and vertical dimensions caudally. The hyperintense posterior epidural fat is defined by anteriorly located, thin, hypointense dura ( black arrows ).

Figure 3–14 Axial CT scan at the mid-thoracic level. The costal facet ( thin black arrow ) on the posterolateral side of the body faces the corresponding head of the rib. Another characteristic of the thoracic vertebrae, the transverse process ( thick black arrow ), articulates with the tubercle of the rib. The pedicle projects posteriorly, and the dural sac is round. The laminae are short and relatively thick.

Pedicles
The stout pedicles of a thoracic vertebra arise from the upper half on the dorsum of the body and pass posterolaterally and slightly inferiorly to the articular pillar and posterior neural arch. On axial MR images or CT scans, the facet joints demonstrate a coronal orientation ( Fig. 3-15 ).

Figure 3–15 The facet joints demonstrate a coronal orientation.

Laminae
The laminae are short and relatively thick. They pass from the articular pillars in a medial and posterior direction. They partly overlap each other from T1 downward (see Fig. 3-14 ).

Spinous Process
The spinous process in the thoracic region is longer and more slender than in the lumbar region and appears triangular in section. The spinous processes of the upper and lower four vertebrae are more bladelike and are directed backward horizontally. The middle four thoracic spines are longer and are inclined downward and backward, so that their spines completely overlap the next lower segments.

Transverse Process
The transverse processes run laterally, superiorly, and posteriorly from the articular pillars. They are closely related to the heads, necks, and tubercles of the corresponding ribs.

Articular Processes
The superior articular processes project upward from the junctions of the pedicles and the lamina on each side, and their facets slant backward and slightly outward. At the inferior edge of the lamina, the inferior articular processes project downward and forward, and their facets face forward, slightly downward and inward.

Intervertebral Foramen
The intervertebral foramen, smaller and more rounded than in the cervical region, is directed laterally at the inferior half of the vertebral body. Its margins are formed by the pedicles superiorly and inferiorly, the vertebral body anteriorly, the neck of the rib anterolaterally, and the facet joints posteriorly. The nerve roots, surrounded by the abundant foraminal fat, are of intermediate signal intensity ( Fig. 3-16 ).

Figure 3–16 The intervertebral foramen is round to ovoid at the inferior half of the vertebral body. Its margins are formed by the pedicles superiorly and inferiorly, the vertebral body anteriorly, the neck of the rib anterolaterally, and the facet joints posteriorly. The nerve roots ( arrows ), surrounded by the abundant hyperintense foraminal fat, are of intermediate signal intensity on this T1-weighted sagittal MR image.

Spinal Canal
The spinal canal is ovoid in cross section, with a relatively large anteroposterior diameter. Epidural fat is abundant posteriorly between the neural arch and the dura, and laterally in the intervertebral foramen. It is, however, less abundant in the anterior half of the epidural space than in the lumbosacral region. The posterior epidural fat demonstrates high signal intensity on T1-weighted and T2-weighted MR images ( Figs. 3-17 to 3-19 ). The posterior longitudinal ligament is difficult to differentiate from the dural sac. Venous sinuses widely occupy the lateral recesses and intervertebral foramina.

Figure 3–17 Epidural fat ( black arrows ) located posteriorly between the neural arch and the dura, and laterally in the intervertebral foramen, demonstrates high signal intensity like the subcutaneous fat tissue on this T2-weighted axial MR image. The back muscles have intermediate signal intensity.

Figure 3–18 Epidural fat ( arrows ) has high signal intensity on a T1-weighted axial MR image.

Figure 3–19 There is little anterior epidural fat. Posterior epidural fat is different from the anteriorly located hypointense dural sac. Ill-defined multiple longitudinal vertical lines in the middle of this MR image represent a motion artifact of the heart.

Conus Medullaris
The conus medullaris, the cone-shaped lower bulging of the spinal cord, projects at the T12-L1 level, and its tip is located at L2-L3. The cauda equina , named for its resemblance to the tail of a horse, is located in the posterior aspect of the canal on axial MR images or CT scans.

The lumbar spine
The lumbar vertebrae , the lowest five of the presacral column, are distinguished by their lack of transverse foramina or costal facets. The lumbar vertebral bodies are large, round or elliptical, and wider from side to side than from front to back. Their upper and lower body margins are flat or slightly concave. They have convex anterior and lateral margins with a flat or concave posterior margin.

Pedicles and Spinous Processes
The pedicles are short and strong, and they project posterolaterally from the upper aspects of the vertebral bodies. They form the upper and lower margins of the neural foramen.
The broad and thick laminae project from the pedicles and meet in the midline to form the spinous process. The large, rectangular spinous processes extend dorsally.

Transverse and Accessory Processes
The flat transverse processes run laterally and slightly posteriorly from the junction of the pedicle ( Fig. 3-20 ). The thick, rounded fifth transverse process sometimes articulates with the iliac bones but also can be fused with the ilium.

Figure 3–20 Axial bone window CT scan of the lumbar spine at the level of the pedicle. Short and thick pedicles project posterolaterally from the upper aspect of the vertebral body. The laminae project from the pedicles and meet in the midline to form the spinous processes. The spinous processes extend dorsally. The flat transverse processes run laterally and slightly posteriorly from the junction of the pedicle. Accessory processes ( arrows ) project from the posterior and inferior surfaces of the bases of the transverse processes.
The accessory processes project from the posterior and inferior surfaces of the bases of the transverse processes.

Articular and Mammillary Processes
The superior articular processes project vertically upward from the articular pillars between the pedicles and the laminae. The concave facet of each superior articular process faces dorsomedially to the inferior articular facets of the vertebra above it ( Fig. 3-21 ). At the inferior aspect of the intervertebral foramen, the superior articular facet becomes contiguous with the pedicle below to form the posterior border of the lateral recess. At this point, the traversing nerve root lies medial to the pedicle, anterior to the superior articular facet, and posterior to the vertebral body and disc [4, 5] . The inferior articular processes run downward and slightly laterally from the laminae. Their articular surfaces face ventrolaterally to the superior articular facets of the vertebrae below them. The articular plane is curvilinear.

Figure 3–21 Axial bone window CT scan of the lumbar spine at the level of the disc. The concave facet of the superior articular processes (S) faces dorsomedially to the inferior articular facets (I) of the vertebra above them. The mammillary processes ( arrow ) projecting backward from the superior articular process are short and round for the attachment of muscles.
The mammillary processes project backward from the superior articular process and are short and round for the attachment of muscles (see Fig. 3-21 ).

Intervertebral Foramina
The intervertebral foramina are defined anteriorly by the posterior vertebral bodies and disc, superiorly and inferiorly by the pedicles, and posteriorly by the articular processes. The intervertebral foramina are the largest in the lumbar area. The spinal ganglia, the spinal branch of the segmental artery, and the sinuvertebral nerve are located in the upper portion of each intervertebral foramen, and the intervertebral veins in the lower portion ( Figs. 3-22 and 3-23 ).

Figure 3–22 T1-weighted sagittal MR image. Note the well-defined intervertebral foramina, which are are largest in the lumbar area. The neural elements ( thick black arrow ) are located in the upper portion of each intervertebral foramen, and the intervertebral veins ( thin black arrow ) in the lower portion.

Figure 3–23 T2-weighted sagittal MR image of the intervertebral foramina. The neural elements and vascular structures are surrounded by hyperintense epidural fat.

Spinal Canal
The spinal canal, which is round or oval at L1, is increasingly triangular toward the lower lumbar vertebrae. It takes on a V shape at the S1 level ( Fig. 3-24 , 3-25 ).

Figure 3–24 The spinal canal, which is round or oval at L1 ( A ), is increasingly triangular toward the lower lumbar vertebrae ( B ). It then takes on a V shape at the S1 level ( C ).

Figure 3–25 Three of the various configurations of the spinal canal.

Meninges
The three layers of meninges (dura mater, arachnoid, and pia mater) that surround the brain also continuously envelop the spinal cord. The dura mater, a dense fibrous tissue extending distally to the S2 segment, is separated from the vertebral canal by an epidural fat layer and a venous plexus. The arachnoid membrane is loosely attached to the dura but is separated from it by a small subdural space. These structures are usually indiscernible from underlying cerebrospinal fluid on CT or MRI. The pia mater is a thin connective tissue closely attached to the spinal cord and its nerve roots.

Epidural Space
The epidural space between the dura and the bones of the spinal canal contains epidural fat, spinal nerves, blood vessels, and ligaments. The epidural fat space is prominent ventral to the dura at the mid-body level of the lumbar vertebrae, especially L5-S1 ( Fig. 3-26 ). The abundant epidural fat makes it easy to differentiate other structures, such as the nerve roots, the venous plexus, and the margin of the discs, on CT and MRI.

Figure 3–26 Axial CT scan at the level of the L5-S1 disc. The dura, the nerve root sheath, the ligamentum flavum, and the disc are well-defined owing to abundant epidural fat. The disc and the ligamentum flavum show mild hyperattenuation in comparison with the dural sac.

Ligaments of the Lumbar Spine
The posterior longitudinal ligament covers the posterior vertebral bodies with some space for the vascular structures. At the level of the intervertebral discs, it attaches tightly to the posterior surface of the anuli of the discs. The ligamentum flavum is 5 mm thick and extends from the anteroinferior border of the lamina above to the upper posterior border of the lamina below. The ligamentum flavum is hyperintense to the bony cortex of the lamina on T1-weighted MR images ( Fig. 3-27 ). Laterally its fibers blend with the thick medial and superior portions of the facet capsule. The anterolateral extension of the ligamentum flavum fuses laterally with the medial portion of the facet joint capsule to reinforce the capsule [6] .

Figure 3–27 The ligamentum flavum is slightly hyperintense to the bony cortex of the lamina on this T1-weighted MR image. Epidural fat is strongly hyperintense to the ligamentum flavum. A small focal hyperintensity ( short thin arrow ) in the posterior midline of the dural sac is due to fatty change of the filum terminale. The dorsal ganglion ( thick arrows ) is isointense to the muscles. The epidural venous plexus appears as punctuate foci of low signal intensity within the hyperintense epidural fat ( long thin arrows ).

Nerves of the Lumbar Spine
The lumbar spinal nerve roots lie in the lateral recess and extend to the medial border of the superior articular facet at the lower portion of the vertebral foramen of the level above. The nerves then pass laterally below the pedicle and enlarge to form the dorsal ganglion (see Fig. 3-27 ). From the ganglion, the peripheral nerves exit laterally out the vertebral foramen.
The nerve roots, which are smaller ventrally and larger dorsally, exit through an intervertebral foramen. The dorsal root becomes the spinal ganglion in the lateral portion of the intervertebral foramen (see Fig. 3-27 ). Lying together, they pierce the dura and unite to form a spinal nerve . The spinal nerves are interconnected with adjacent sympathetic trunk ganglia by rami communicantes , providing an explanation for the mutual overlapping of segmental sensory nerve distribution. Small recurrent meningeal branches originate from the spinal nerves shortly after emerging from the intervertebral foramina, and they innervate the meninges and their vessels. Then the spinal nerves divide into the ventral and dorsal rami. The ventral rami supply the anterior and lateral parts of the trunk. The dorsal rami turn backwards to supply the cutaneous and muscular regions and the facet joints ( Fig. 3-28 ).

Figure 3–28 The spinal nerves divide into the ventral and dorsal rami. The ventral rami supply the anterior and lateral parts of the trunk. The dorsal rami turn backwards to supply the cutaneous and muscular regions and the facet joints.

Lumbar Venous Plexus
The epidural venous plexus appears as punctuate foci of low signal intensity within the hyperintense epidural fat (see Fig. 3-27 ).
The basivertebral veins , from the cancellous vertebral bodies, drain into the anterior internal vertebral plexus in the midportion of the posterior vertebral body. They also drain into the anterior external plexus through many openings in the anterior and lateral surfaces of the vertebral body. Two external vertebral plexuses, anterior and posterior, existed as follow; The anterior external plexus lies in the anterior surface of the vertebral bodies. The posterior external plexus lies over the vertebral laminae and extends around the vertebral processes.

Lumbar Disc
The intervertebral disc in the lumbar region has three parts: the cartilaginous end plate, the anulus fibrosus, and the nucleus pulposus [7] . The intervertebral discs are thickest in the lumbar region. Lumbar lordosis is due to the increase in differential between the anterior and posterior thicknesses of the discs, a situation that makes the lumbosacral disc the most wedge shaped [8] . On axial sections, the upper four lumbar discs have a slightly concave or flat posterior border, conforming to the adjacent V-shaped bodies. The fifth lumbar disc, however, has a flatter, slightly convex posterior border ( Fig. 3-29 ).

Figure 3–29 T2-weighted axial MR images. The L2-L3 disc ( A ) has a slightly concave border, and the L3-L4 ( B ) and L4-L5 discs ( C ) become flatter at their posterior borders. ( D ) The fifth lumbar disc has a flatter, slightly convex posterior border.
The cartilaginous end plate is composed of hyaline cartilage that covers the upper and lower vertebral body surfaces. The end plate in the adult lumbar spine is avascular; however, it serves as a biomechanical and metabolic interface between the vertebral body and the nucleus pulposus. There it becomes the main site of diffusion in the vertebral body. The anulus fibrosus, the outer, circular, collagenous and fibrous layer, attaches to the vertebral body and to the anterior and posterior longitudinal ligaments.
The nucleus pulposus is composed of very hydrated and loose fibrous strands with the consistency of a gel. The nucleus pulposus usually blends with the anulus fibrosus without demarcation between the two. The nucleus consists of 85% to 90% water, and the anulus 80% water [9] . On T1-weighted MR images, the nucleus pulposus and the anulus fibrosus show slightly lower signal intensity and they cannot be separated ( Fig. 3-30 ). On T2-weighted MR images, however, the nucleus pulposus demonstrates high signal intensity and the anulus demonstrates low signal intensity. However, the central cleft is low in intensity on T2-weighted MR images owing to the abundance of collagen fiber.

Figure 3–30 A, T1-weighted sagittal image showing that the nucleus pulposus and the anulus fibrosus are slightly hyperintense to the cortical bone. However, those two structures are not delineated. The anterior epidural fat becomes abundant in the lower lumbar vertebrae, especially at the L5-S1 level. B, On the T2-weighted sagittal image, the nucleus pulposus demonstrates high signal intensity, and the anulus demonstrates low signal intensity. However, the central cleft is low in intensity owing to the richness of collagen fiber.
The cortical bone shows markedly low signal intensity and is easy to differentiate from the hyperintense bone marrow. The disc is hyperdense to the psoas muscle on CT (see Fig. 3-26 ).

Lumbar Arteries and Veins
The upper four paired segmental lumbar arteries arising from the abdominal aorta supply the lumbar spine. The radiculomedullary branches supply the dural sac and its contents. The fifth lumbar arteries often arise from the sacral artery, but their origin is variable. Two longitudinal internal vertebral plexuses, anterior and posterior, and their many smaller transverse communicating veins form the networks of veins in the epidural space within the spinal canal.

References

1 Fielding J.W., Hawkins R.J. Atlanto-axial rotatory fixation. J Bone Joint Surg Am . 1977;59:37-44.
2 Parke W.W., Schiff D.C.M. The applied anatomy of the intervertebral disc. Orthop Clin North Am . 1971;2:309-324.
3 Flannigan B.D., Lufkin R.B., McGlade C., et al. MR imaging of the cervical spine: Neurovascular anatomy. AJR Am J Roentgenol . 1987;148:785-790.
4 Dorwart R.H., Sauerland E.K., Haughton V.M., et al. Normal lumbar spine. In: Newton T.H., Potts D.G., editors. Computed Tomography of the Spine and Spinal Cord . San Anselmo, CA: Clavadel; 1983:93-114.
5 Schnitzlein H.N., Murtagh F.R. Imaging Anatomy of the Head and Spine. Baltimore: Urban & Schwarzenberg, 1985.
6 Grenier N., Kressel H.Y., Schiebler M.L., et al. Normal and degenerative posterior spinal structures: MR imaging. Radiology . 1987;165:517-525.
7 Coventry M.B. Anatomy of the intervertebral disc. Clin Orthop Relat Res . 1969;67:9-15.
8 Parke W.W., Schiff D.C.M. The applied anatomy of the intervertebral disc. Orthop Clin North Am . 1971;2:309-324.
9 White A.A., Gordon S.L. Synapsis: Workshop on idiopathic low-back pain. Spine . 1982;7:141-149.
Chapter 4 Imaging Diagnosis of the Degenerative Spine

In-Sook Lee, MD

Conventional radiography (plain films)
The role of conventional radiography in diagnosing spinal pain is to assess the alignment and position of the spinal structures. Findings from plain films can, therefore, identify degenerative narrowing of the intervertebral discs, subchondral sclerosis, and osteophyte formation. The accepted rule of thumb for assessing the spacing of the vertebra with plain films is that the height of a given lumbar intervertebral disc space should always be slightly greater than the height of the disc space one level above it ( Fig. 4-1 ) [1] . This rule does not apply to the transition disc immediately above the sacrum (usually L5-S1).

Figure 4–1 Plain lateral radiograph of the lumbar spine. Normally, the height of the L2-L3 disc space at is slightly greater than that of the L1-L2 disc space by the accepted rule of thumb. The height of the L3-L4 disc space is slightly less than that of the L2-L3 disc space, and the height of the L4-L5 disc space is less than that of the L3-L4 disc space. In a MR image taken of the same patient, there were disc bulges at L3-L4 and L4-L5 (not shown).

Intervertebral Osteochondrosis
Loss of disc space and bony sclerosis of the adjacent vertebral bodies are the radiographic manifestations of disc degeneration; these findings collectively have been termed intervertebral osteochondrosis ( Fig. 4-2 ). With progression of intervertebral osteochondrosis, there is pathologic evidence of the following abnormalities:
Enlarging clefts
Diminution of the disc space
Bulging of the outer fibers of the anulus fibrosus
Destruction of the cartilaginous end plates
Thickening of adjacent trabeculae

Figure 4–2 Intervertebral osteochondrosis. Plain lateral radiograph of the lumbar spine shows narrowing of the disc space at L2-L3 and L3-L4 as well as bony sclerosis of the adjacent vertebral bodies. Also, there are multiple anterior projecting osteophytes at the vertebral end plates (spondylosis deformans).
Disc space loss and bony sclerosis are commonly seen together on radiographic images. The sclerotic zones are variable in size, are commonly triangular, and involve both vertebral bodies that border the narrowed intervertebral disc. These radiographic and pathologic findings in intervertebral osteochondrosis can be apparent at any level in the spine; however, abnormalities are found predominantly in the lower lumbar and cervical regions [2] . In most situations, narrowing of an intervertebral disc space in the absence of other evidence of chronic discopathy is the only detectable sign suggesting a disc herniation at the lumbar spine [1] .

Spondylosis Deformans
Spondylosis deformans is osteophytosis of the end plates (see Fig. 4-2 ). It is thought to be secondary to anterolateral disc displacement, which results in traction at the site of osseous attachment (Sharpey fibers) of the anulus [2, 3] . The presence of posterior or foraminal vertebral body osteophytes, whether or not associated with disc space narrowing, is a definite sign of a chronic disc herniation [2] . With the development of more severe degenerative changes, the disc space narrows and radiolucent interspace accumulations of gas develop at sites of negative pressure; this is referred to as vacuum disc phenomenon ( Fig. 4-3 ) [2, 4] . Calcification of the intervertebral disc may also be seen ( Fig. 4-4 ) [5] . Central spinal canal stenosis is difficult to evaluate, and soft tissues cannot be directly visualized on plain films.

Figure 4–3 Vacuum disc phenomenon. This plain lateral film of the lumbar spine shows marked narrowing of the disc space and sclerosis of the adjacent end plates at L4-L5. There is a radiolucent accumulation of gas ( arrow ) within the disc space.

Figure 4–4 Plain lateral radiograph of the thoracic spine demonstrates multiple calcifications ( arrows ) within the intervertebral disc spaces.

Myelography
Historically, the roles of myelography has been to enable (1) differentiation among the thecal sac, spinal cord, and exiting nerve roots and (2) determination whether these structures are compromised by disc bulging, disc herniation, or spinal stenosis [3] . Disc herniations can be demonstrated only indirectly [1] . They are diagnosed on the basis of features such as [6] :
Indentation of the column of contrast agent ( Fig. 4-5 )
Distortion of the nerve roots
Asymmetric filling of nerve root sleeves

Figure 4–5 Plain myelograms ( A and B ) and CT myelograms ( C and D ). A, Normal plain myelogram of the lumbar spine level. B, Plain lateral myelogram showing multifocal indentations of the column of contrast agent at the disc levels. C and D, On axial CT myelograms, contrast material within the subarachnoid CSF space is not clearly visible at the disc level owing to extensive disc bulging ( D ), unlike at the vertebral body level ( C ).
Plain myelography easily enables coverage of the entire lumbar area and assessment of the intrathecal structures (cauda equina and conus medullaris). However, far lateral foraminal herniations, extraforaminal herniations, and anterior herniations cannot be detected on myelography [1] . Therefore, this modality is a less sensitive diagnostic tool for the detection of lateral disease, and it cannot specifically enable diagnosis of the nature of extradural disease [ 7 - 9 ]. Myelography today is usually performed in conjunction with computed tomography (CT) (see Fig. 4-5 ). Myelography remains an invasive procedure that adds little, if anything, to the evaluation of degenerative disc disease in comparison with CT or magnetic resonance imaging (MRI) [10] .

Computed tomography
CT has the distinct advantages of being noninvasive and of providing direct anatomic information [11] . CT scans can, therefore, demonstrate the intervertebral disc directly [3] and can enable diagnosis of disc herniation and degenerative stenosis without the use of contrast material. However, CT is relatively insensitive to the primary derangement of degeneration, because in the early stages of the disorder, the configuration of the disc itself is not changed. This shortcoming may result in an underestimation of the severity of degenerative changes within the nucleus pulposus and anulus fibrosus on CT scans [12] .
Although largely supplanted by MRI, CT is often still used in the following three situations [6] :
When the patient has implants (e.g., aneurysm clips, pacemaker)
As an adjunct to myelography, particularly in the evaluation of spinal stenosis
To evaluate the relative contributions of calcification/bone and soft tissue in a lesion discovered on MRI
CT represented a major advance in the evaluation of disc disease because its ability to distinguish soft-tissue from bone changes drew attention to the sequelae of disc degeneration, such as stenosis, facet joint disease, and ligamentous hypertrophy [13, 14] . The following reactive changes or secondary reflections of degeneration are noted on CT [3] :
Anular bulging
Herniation
Calcification
Vacuum phenomenon
Sclerosis of the adjacent intervertebral body ( Fig. 4-6 ) [3]
The presence of gas in the herniated material [2]
Bony overgrowth
Marginal sclerosis
Cyst formation
Facet joint narrowing [3]

Figure 4–6 Reactive changes at vertebral bodies on CT scans. A, The findings of disc bulging with vacuum phenomenon and joint space narrowing as well as subchondral sclerosis with cysts at the facet joint are shown on this axial CT scan. Determining of the precise degree of central canal stenosis is relatively difficult. B, Osteophytes are projected from the bony cortex at the adjacent end plate.
Calcifications within the displaced disc material are readily seen, but it may be difficult at times to differentiate calcification from an accompanying osteophyte or a bone fragment avulsed from the vertebral body ring epiphysis. The major disadvantages of CT stem from limitations in contrast agent sensitivity between various soft tissues and from the limited field of view [3] .

Discography
Discography is a reliable means of evaluating the integrity of the intervertebral disc. The purpose of the intradiscal injection is primarily the demonstration of an anular tear, and the degenerative disc is often injected without difficulty [4] . When a disc herniation has been diagnosed with other imaging modalities, discography can show whether the herniation is contained or noncontained [1] . Extravasation of contrast medium occurs within fissures in the anulus fibrosus and may be seen in cases of degeneration and herniation [15, 16] . When coupled with a CT examination, discography provides excellent delineation of the exact location of fissures and defects in the anulus fibrosus as well as herniation [3] .

Magnetic resonance imaging
MRI is currently the imaging technique of choice for the evaluation of degenerative changes of the spine [6] . It provides a better assessment of disc morphology than CT scanning or CT myelography [1] . The contrast sensitivity and multiplanar imaging capability of proton MR imaging make this modality a unique noninvasive means of imaging the intervertebral disc. From a morphologic aspect, MRI may be the most accurate means of evaluating the intervertebral disc [3] .

General considerations in degenerative joint disease

The Cervical Spine
The most common locations for degenerative changes to occur are in the lower cervical spine, particularly at the C5-C6 interspace. Below the atlantoaxial joint, each segment has three joint complexes, the apophyseal joint, the uncovertebral joint, and the intervertebral disc, that can potentially undergo degeneration either separately or simultaneously.

Apophyseal (Facet) Joints
Degeneration of apophyseal joints, found predominantly in the middle and lower cervical spine, is characterized by fibrillation and erosion of articular cartilage, partial or complete denudation of the cartilaginous surface, and new bone formation. Facet arthrosis is has the following characteristics [3] :
Loss of joint space
Subchondral sclerosis
Osteophytes
Anterolisthesis (degenerative spondylolisthesis)
Most diagnostic radiographs are frontal (anteroposterior [AP]) or oblique projections. On an AP projection, the normally smooth lateral contour of the articular pillars shows sharp osteophytic projections and sclerosis in cases of facet joint degeneration. The oblique projection may demonstrate posterior foraminal encroachment from protruding osteophytes ( Fig. 4-7 ) [17] .

Figure 4–7 Facet arthrosis. A, Anteroposterior radiograph of the cervical spine shows irregular joint space narrowing and mild subchondral sclerosis ( arrows ) at the left side of the C3-C4 facet joint. B, Oblique plain film demonstrates posterior foraminal encroachment from protruding osteophytes ( arrows ). With foraminal narrowing, there is a loss of normal teardrop shape, and the foraminal configuration has an hourglass appearance. C, On an axial CT scan of the C3-C4 level, large irregular osteophytes, narrowing of the joint space, and ill-defined sclerosis are shown.

Uncovertebral Joints (Joints of von Luschka )
Uncovertebral ( neurocentral ) joints show a predilection for degenerative changes in the lower segments of C5 and C6. Anatomically, they occupy the posterolateral portions of the vertebral bodies, contributing to the anterior border of the intervening intervertebral foramen and lateral recess. As disc height diminishes because of degeneration of the cervical intervertebral disc, the bone protuberances around the uncovertebral articulations approach each other and are pressed firmly together [2] .
Degenerative changes consist predominantly of osteophyte formation, particularly at the uncinate process. This change is optimally observed on AP and oblique projections. The AP projection shows an initial sharpening of the tip of the uncinate process with a progressive bulbous enlargement, especially in a lateral direction. Oblique views frequently reveal uncovertebral arthrosis with osseous foraminal encroachment in a patient for whom AP and lateral views appear normal ( Fig. 4-8 ) [17] . Osteophytes of uncovertebral origin invariably project directly posteriorly into the anterior aspect of the intervertebral foramen, creating stenosis of the adjacent lateral recess, and at times may interfere with vertebral artery blood flow [18, 19] . The combination of anterior uncovertebral and apophyseal joint arthrosis may result in a foraminal configuration analogous to that of an hourglass (see Fig. 4-7 ).

Figure 4–8 Arthrosis of uncovertebral joint. A, Anteroposterior projection shows bulbous enlargement of the tip of the uncinate process ( arrows ) in a lateral direction at the level of C4-C5. B, Oblique view demonstrates osseous foraminal encroachment by posteriorly projected osteophytes ( arrows ). C, Abnormal bony proliferation, multiple small subchondral cysts, and joint space narrowing can be seen at the right side of the uncovertebral joint, causing a narrowing of neural foramen on this axial CT scan.
The degree of anatomic reduction in foraminal dimensions cannot be accurately assessed because of a 1- to 3-mm radiolucent cartilage cap. This limitation accounts for the frequent discrepancy between radiographically visible degenerative changes and directly related clinical abnormalities [19] . CT scanning with the bone window setting remains the optimum method for accurate assessment, although MRI using thin sections may be almost as accurate [20] .

Intervertebral Disc
Degeneration of the intervertebral disc (spondylosis) most commonly occurs at levels C5 and C6 . The common signs of intervertebral disc degeneration are loss of disc height, presence of osteophytes, and end plate sclerosis ( Fig. 4-9 ). An occasional accessory sign is the vacuum phenomenon, which is more frequently observed in the lumbar spine. The appearance of a lucent vacuum cleft adjacent to an end plate on an extension film after trauma may indicate anular tearing [21] .

Figure 4–9 Degeneration of an intervertebral disc. A, Plain lateral radiograph shows narrowing of disc space and anterior osteophytes at the C5-C6 level. B, Sagittal T2-weighted MR image shows abnormal low signal intensity representing disc degeneration and disc bulging at the same level.
The most reliable sign of disc degeneration is the loss of disc height in varying degrees. Above the degenerating disc, lordosis is frequently diminished [19] . In the absence of visible disc disease, osteophytes initially may be nonmarginal in origin as well as large. However, the combination of loss in disc height and osteophyte formation is usually isolated to the involved level. Anteriorly projecting osteophytes rarely cause dysphagia [22] . Posterior osteophytes projecting into the spinal canal are usually smaller, owing to their posterior longitudinal ligament (PLL) attachment, but they can produce central canal stenosis with resultant myelopathy ( Fig. 4-10 ) [23] . Another prominent sign of disc degeneration often observed is a varying degree of end plate sclerosis , occasionally extending into the midportion of the vertebral body. This finding may simulate an osteoblastic neoplasm or infection. Sclerosis beneath an osteophyte may simulate the inflammatory sclerosis of ankylosing spondylitis. The key to differential diagnosis in degenerative joint disease is to observe the adjacent end plate and the associated loss of disc space. If the vacuum phenomenon is present and the cortical continuity of the end plate is intact, the condition is very likely to be degenerative rather than infective [17] .

Figure 4–10 Compressive myelopathy of spinal cord. A, Right parasagittal T2-weighted MR image shows a posterior osteophyte ( arrow ) of the C5 vertebral body as well as C5-C6 disc protrusion. B, Central canal stenosis and abnormal high signal intensity within the spinal cord are shown on the central sagittal T2-weighted MR image. This finding represents compressive myelopathy by disc herniation and osteophyte formation.

The Thoracic Spine

Apophyseal (Facet) Joints
Although degeneration of the facet joints is infrequently observed in the thoracic spine, it is most often seen in the upper thoracic and mid-thoracic spine . Radiographic findings indicating degeneration of the facet joints include joint space narrowing, bone eburnation, and osteophytosis. The changes are best observed on AP views [2, 17] .

Costal Articulation
The ribs and vertebral column articulate at two areas, between the heads of the ribs and the vertebral bodies (costovertebral) and between the necks and tubercles of the ribs and the transverse processes of the vertebrae (costotransverse). Both of these areas are synovial articulations and, therefore, are subject to osteoarthritis [2] . Degenerative changes are most commonly found in the lower thoracic segments, especially in the articulations of the 11th and 12th ribs . Arthrosis of these articulations is indicated by the same features seen with degenerative changes at other joints—joint space narrowing, bone eburnation, and osteophytes [17] . These features are evident although their radiographic demonstration is difficult ( Fig. 4-11 ).

Figure 4–11 Degeneration of costal articulation. Axial CT scans show subchondral sclerosis ( arrows ) at costotransverse articulation ( A ) and large osteophytes ( arrows ) at the costovertebral articulations ( B ). C, Plain AP radiograph of the thoracic spine shows osteophytes ( arrows ) at multilevel costotransverse joints.

Intervertebral Disc (Spondylosis, Senile Kyphosis)
Degenerative disc changes are less pronounced in the thoracic spine than in other spinal regions. Developmentally, the height of normal thoracic disc spaces gradually decreases in a cephalad direction, with the thinnest disc interspaces present between the T2 and T4 regions. The most common sites for disc-related degenerative changes to occur are the middle and lower thoracic levels. The major radiographic features in the thoracic spine are osteophytes, minimal sclerosis, and mild disc narrowing [17] . There is a notable absence of osteophyte formation on the left side of the thoracic spine, which is presumably related to the inhibition of bone production owing to the pulsations of the descending aorta on the left side ( Fig. 4-12 ) [2, 24, 25] . Infrequently, usually in the elderly, degeneration of the anterior fibers of the anulus fibrosus in multiple segments in the mid-thoracic spine may lead to ankylosis across the anterior disc space, with an associated localized kyphosis (senile kyphosis) [26] . Senile kyphosis is most common in men who do not demonstrate osteoporosis. Radiographic findings include progressive kyphosis in the mid-thoracic spine, disc ossification, and eburnation of the vertebral bodies [2] .

Figure 4–12 Disc-related degenerative changes of the thoracic spine on plain radiographs. A, Lateral view shows multiple anterior osteophytes and mild disc space narrowing at middle and lower thoracic spine levels; the kyphotic curvature is relatively increased. B, There is a notable absence of osteophyte formation on the left side of the thoracic spines on an AP view.

The Lumbar Spine

Apophyseal (Facet) Joints
The most common location for degeneration of the facet joints is the lower lumbar spine . Arthrosis in this location is characterized by a loss of joint space, the presence of osteophytes, sclerosis, and subluxation . Facet arthrosis may produce anterolisthesis and, less frequently, retrolisthesis of an individual segment.
The best diagnostic projections are the AP and oblique films, although degenerative spondylolisthesis and intersegmental instability may require lateral films in flexion and extension ( Fig. 4-13 ) [17] . The AP film shows a loss of joint space , which nevertheless is an unreliable sign in this projection owing to common anatomic variations in facet planes and projectional distortion. Sclerosis may be evident in the subchondral bone. Osteophytes usually arise at the superior aspect of the joint, but they too are difficult to identify. By far the best diagnostic film is the oblique view, which allows accurate visualization of most of the lumbar apophyseal joints. Less than 25% of degenerative facets visible on CT appear on oblique radiographs [27] . Often, degenerative facet subluxation is evidenced as subchondral sclerosis in the adjacent pars region, which is mechanically impacted, particularly at L4 and L5 [17] . The lateral radiograph may reveal an increase in density in the region of the apophyseal joints, but this appearance is often an artifact of the decreased beam penetration through the overlying pelvis. An additional common radiographic projectional artifact seen at the L4 and L5 levels is the superimposition of the superior articulating process into the foramen, simulating osseous encroachment [17] .

Figure 4–13 Lumbar facet arthrosis with degenerative spondylolisthesis. Plain AP ( A ) and left oblique ( B ) radiographs show the narrowing of joint space ( arrows ) at the left side of the L4-L5 facet joint. There is abnormal widening of right facet joint space ( open arrow ) at the L4-L5 level. Lateral extension ( C ) and flexion ( D ) views of the lumbar spine well show the dynamic anterolisthesis at the L4-L5 level. E, Axial CT scan of the L4-L5 level demonstrates osteophytes, vacuum phenomenon, joint space narrowing ( left ) and joint subluxation ( right ) at both facet joints, along with the accompanying disc bulging.
Because the capsule and ligaments of the apophyseal articulations are richly supplied with nerves, prominent clinical manifestations of osteoarthritis in these locations are expected. Furthermore, the occurrence of various types of spinal stenosis in this disease, leading to compression of the spinal cord and nerve roots, is well recognized and best demonstrated by means of CT [2] .

Intervertebral Disc
The most common location for disc degeneration is at the L4-L5 level. As in the cervical spine, the major radiographic signs consist of decrease in disc height, osteophyte formation, end plate sclerosis, vacuum phenomenon, and subluxation ( Fig. 4-14 ) [17] . The best diagnostic radiograph for the detection of degenerative disc disease is the lateral projection, supplemented with AP and oblique studies.

Figure 4–14 Degeneration of a lumbar intervertebral disc. Plain lateral radiograph shows narrowing of the disc space, subchondral sclerosis of the adjacent end plates, and anterior traction bony spurs at the L4-L5 level.
The early signs of a degenerating disc are retrolisthesis, mild loss of disc height, small anterior traction spurs, and vacuum phenomenon. Retrolisthesis often occurs early, with loss of disc height, owing to the posterior orientation of the apophyseal joints; the segment is drawn posteriorly as it is displaced inferiorly [17] . A wide apophyseal joint space or an offset in the articular surfaces, as seen in the oblique projection, has been implicated as an early sign of degenerative disc disease (see Fig. 4-13A ) [28] .
The primary radiologic and pathologic finding in spondylosis deformans is osteophytosis, an abnormality that becomes increasingly common in each successive decade of life. According to Schmorl and other investigators, including Hilton and colleagues [26, 29] , abnormalities in the peripheral fibers of the anulus fibrosus are the initiating factors in spondylosis deformans. This discontinuity results in weakening of the anchorage of the intervertebral disc to the vertebral body and allows anterolateral disc displacement. Displacement of the intervertebral disc may lead to traction at the site of osseous attachment (Sharpey fibers) of the anulus fibrosus (or short perivertebral ligaments) [30] to the vertebral surface. Osteophytes develop several millimeters from the discovertebral junction. There are usually two types of osteophytes, traction and claw ( Fig. 4-15 ) [31] . Traction osteophytes , which occur in the early phase of disc degeneration, are horizontal and are tapered at their distal extents [32] . They typically originate about 2 mm from the anterior vertebral body margin. Posterior body osteophyte formation is infrequent in the lumbar spine because of a less adherent PLL and anulus fibrosus. Claw osteophytes have a broader base, climb vertically in a curvilinear fashion, and are tapered. They appear to be derived from a traction spur once shear forces have diminished to more compressive loads [31] .

Figure 4–15 Osteophytes of vertebral bodies. A, Traction osteophytes. Their origin is nonmarginal and they tend to be horizontal and tapered at their distal extents ( arrows ). B, Claw osteophytes. Also tending to be nonmarginal and to project horizontally, these osteophytes have a broader base and are larger, curve superiorly or inferiorly, and taper distally ( arrows ).
Large osteophytes may completely bridge the intervertebral disc space or may be in close apposition to the adjacent segment. Such an osteophyte exhibits a broad base that extends from the vertebral body margin to a few millimeters away. The distal extension of the osteophyte exhibits a gentle curve laterally and either superiorly or inferiorly, gradually tapering to a slightly rounded, pointed apex, with the appearance of an animal’s claw (claw osteophyte). Such a claw osteophyte is best seen on the anterior or lateral body margin (see Fig. 4-15 ) [32] . These degenerative bony excrescences are to be distinguished from the following bony structures:
The syndesmophytes of ankylosing spondylitis, which appear as slender, vertically oriented excrescences extending from the margin of one vertebral body to its neighbor ( Fig. 4-16 )
The paravertebral ossifications of psoriasis and Reiter syndrome, which are sweeping bone excrescences involving the lateral aspect of intervertebral discs and vertebral bodies in an asymmetric fashion
The flowing ossifications of diffuse idiopathic skeletal hyperostosis (DISH) ( Fig. 4-17 ) [2]

Figure 4–16 Diffuse syndesmophytes of ankylosing spondylitis. There are multiple vertical thin osteophytes ( arrows ) with smooth margins that are forming bridges between vertebral bodies and are distributed symmetrically. These syndesmophytes are different from degenerative bony excrescences.

Figure 4–17 Diffuse idiopathic skeletal hyperostosis (DISH). A continuous uneven contour (bumpy contour) caused by exuberant hyperostosis can be seen at the anterior aspect of vertebral bodies in the thoracolumbar spine. Complete anterior bridging has occurred at every disc level. These ossifications are different from claw osteophytes which is due to spondylosis deformans.
The vacuum sign of Knutsson is an important early radiographic finding [4] . It is essentially composed of pockets of nitrogen gas in the nuclear pulposus and anular fissures, and it appears as an area of linear radiolucency in the disc space [33] . Studies have shown this finding to be a common sign of disc aging and degeneration, with an incidence of 2% to 3% in the general population [34] . The collection of nitrogen in the discal fissures is thought to originate from adjacent extracellular fluid. In movements of the spine that lower the pressure in the disc, such as in extension, nitrogen is released from the adjacent extracellular fluid and accumulates in the discal fissures because of the pressure gradient. Therefore this collection of gas can be made to disappear with spinal flexion and to reappear with spinal extension ( Fig. 4-18 ).On MRI, the disc shows diminished signal intensity owing to dehydration and a signal void at the vacuum site [4] .

Figure 4–18 Vacuum phenomenon. A, On a flexion radiograph, intradiscal gases are almost obliterated. B, On an extension radiograph in the same patient, multilevel vacuum phenomena ( arrows ) are more apparent. An extension view is the best one to reveal a vacuum.
Spinal subluxations are more readily recognizable. These lateral, anterior, and posterior vertebral body displacements can occur in measurable degrees. Flexion-extension films usually reveal decreased motion in the displaced segments. Disc height is markedly diminished, with greater than 25% loss in the vertical dimension. Loss of disc height can also be due to infection, which should be ruled out through careful scrutiny for the loss of the vertebral body end plates [17] .

The Sacroiliac Joints
The joint between the articular surfaces of the sacrum and ilium is synovial in type. A cartilaginous surface is present in both the sacrum and the ilium, being considerably thicker on the sacral aspect of the joint [35] . The joint possesses a complete fibrous capsule and is lined with a synovial membrane. It is important to realize that only the lower one half to two thirds of the space between the sacrum and the ilium represents the synovial articulation ; the superior aspect of the space is ligamentous .
Pathologic evidence of degenerative abnormalities of the sacroiliac articulation is common and prominent, especially in the ilium, in middle-aged and elderly individuals [35] . The abnormalities may be unilateral or bilateral in distribution. Erosion and fibrillation of cartilage, sloughing of necrotic material, and partial or complete fibrous ankylosis of the joint are seen. Bony sclerosis and osteophytosis are most common on the anterior articular surface, and the latter can lead to para-articular ankylosis owing to the presence of bridging osteophytes ( Fig. 4-19 ).

Figure 4–19 Degeneration of the sacroiliac joint. A. Mild subchondral sclerosis ( arrows ) and small subchondral cyst is seen predominantly at the iliac bones. B. Osteophyte ( arrow ) is more common on the anterior articular surfaces of the sacroiliac joint on axial CT scans of the pelvis. C, Mild sclerotic change ( arrow ) around the anterosuperior aspect of the right sacroiliac joint is suspicious on a plain pelvis radiograph. Radiographic evaluation of this joint is made difficult by the undulating contour of apposing articular surfaces.
Radiographic evaluation of the sacroiliac joint is difficult because of the undulating contours of apposing articular surfaces ( Fig. 4-19 ). Although CT is an established method for the evaluation of traumatic, neoplastic, and infectious alterations around the sacroiliac joint, this modality is generally not required in the diagnostic assessment of osteoarthritis or other articular processes in this location. With regard to osteoarthritis, CT delineates the para-articular nature of the osseous proliferation [3] .

Disc degeneration and internal disc disruption
The volume of the intervertebral disc tissue decreases with degeneration [3] . Nachemson and colleagues [36] , reporting on a relatively small number of lumbar discs, showed that old age and disc degeneration are not necessarily linked and also that disc degeneration is not synonymous with disc thinning. Twomey and Taylor [37] distinguished between “normal” age change and “pathological” disc degeneration. These distinctions were described as grade 2 and grade 3 degeneration, respectively, by Rolander [38] . Grade 2 degeneration is characterized by a less distinct boundary between the nucleus and anulus and a color change from white to yellowish brown. There may be an isolated fissure in the anulus. Grade 3 degeneration is characterized by frank disc degeneration with desiccation, multiple fissures in nucleus and anulus, and disc thinning. Only grade 3 degeneration involves disc thinning and desiccation. The cause of disc degeneration is as yet unknown. Possible causes of disc thinning are the loss of disc material due to herniation and the loss of volume due to dehydration [37] .
The term disc degeneration has been used to indicate various histopathologic processes and radiographic findings, including disc narrowing, dehydration, anular fissures, and subchondral bone marrow changes [3, 4] . Degenerated nucleus pulposus is characterized by the absence of fibrocartilage, the disruption of anular fibers, the narrowing of the disc space, and the presence of osteophytes. Also, radial tears can be found as well as the replacement of fibrocartilage by collagen or fluid [39] .

Disc Dehydration and Narrowing
Usually, disc dehydration accompanies disc space narrowing. Height determination requires comparison either with other levels in the same patient or with other patients [6] . The deteriorated disc is characterized by the following :
Narrowing of the intervertebral space
Irregular disc contour generally associated with symmetric or asymmetric bulging
Abundant presence of gas in the central portion of the intervertebral disc space
Multidirectional osteophytes that do not avoid the central spinal canal or the foramina
End plate erosions with reactive osteosclerosis
Chronic bone marrow changes [1]
Biochemical changes in the nucleus pulposus are related to a decrease in water-binding capacity, disintegration of large molecular proteoglycans, and an increase in collagen content [40] . The onion-skin edges of the nucleus pulposus begin to unravel, and cracks, clefts, or cervices appear within the nucleus and extend into the anulus fibrosus [2] . Deteriorated discs represent real pathologic degeneration, which is sometimes referred to as chronic discopathy . On microscopic examination, such discs show total structural disorganization and general replacement of normal disc material by scar tissue [1] .

Magnetic Resonance Imaging and Disc Degeneration
MRI demonstrates degenerative changes in not only disc contour but also internal disc morphology. Good quality, spin-echo T2-weighted MR images provide contrast between the nucleus pulposus and the outer anulus of normal discs. Signal intensity is proportional to the water content of the proteoglycan matrix of the disc [ 41 - 44 ]. On MRI, disc degeneration is evidenced by a decreased signal intensity of the disc and a diminished separation of the nucleus pulposus from the anulus fibrosus. With complete degeneration, the signal intensity is markedly decreased, and the nucleus and anulus are inseparable ( Fig. 4-20 ) [45] .

Figure 4–20 Disc dehydrations. Sagittal T2-weighted MR image shows variably decreased signal intensity of discs from L2-L3 to L5-S1. The separation of the nucleus pulposus from the anulus fibrosus is less complete at L2-L3 and L3-L4, representing mild dehydration. At the level of L5-S1, signal intensity is markedly decreased and the nucleus pulposus and anulus fibrosus are inseparable; this finding indicates severe dehydration. Degenerative disc bulging and loss of disc height at L4-L5 and L5-S1 can also be seen. Numbers 1 through 5 indicate lumbar vertebrae.
The signal intensity of the disc on T2-weighted MR images reflects fibrocartilage, collagen, and fluid content. The presence of fibrocartilage is correlated with a high signal, and the presence of dense collagenous fibrous tissue with a low signal. Therefore, replacement of fibrocartilage by amorphous collagen results in a lower signal intensity, and replacement by fluid-filled cystic spaces results in a higher signal intensity [39] .
Through signal reduction, spin-echo T2-weighted MR images reveal degradation of the matrix in diseased discs. In the case of severely degenerated discs in which the overall signal intensity is decreased, there may be linear areas of high signal intensity, which are thought to represent free fluid within cracks or fissures of the degenerated complex ( Fig. 4-21 ) [3] .

Figure 4–21 Free fluid within the severely dehydrated disc. Sagittal T2-weighted MR image shows narrowing of the disc space and overall low signal intensity of the disc at L4-L5. There is abnormal linear high signal intensity ( arrow ) within the dehydrated disc. Numbers 4 and 5 indicate lumber vertebrae.
Disc signal intensity exists as a cont

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