painful hip - aanem

��American Association of Neuromuscular & Electrodiagnostic Medicine

Jeffrey S. Brault, DO

Lyell K. Jones, MD

Keith Bengtson, MD

Raza A.Awan, MD

PAINFUL HIP

2005 AANEM COURSE DAANEM 52ND Annual Scientific Meeting

Monterey, California

2005 COURSE DAANEM 52nd Annual Scientific Meeting

Monterey, California

Copyright © September 2005American Association of Neuromuscular & Electrodiagnostic Medicine

421 First Avenue SW, Suite 300 EastRochester, MN 55902

PRINTED BY JOHNSON PRINTING COMPANY, INC.


Lyell K. Jones, MD

Keith Bengtson, MD

Raza A.Awan, MD

Painful Hip

��

Painful Hip

Faculty

ii


Assistant Professor

Department of Physical Medicine and Rehabilitation

Mayo Clinic College of Medicine

Rochester, Minnesota

Dr. Brault earned his degree from the Chicago College of OsteopathicMedicine at Midwestern University and performed a residency in physicalmedicine and rehabilitation at the Mayo Graduate School of Medicine. Heis presently an assistant professor of physical medicine and rehabilitation,and a consultant in the Department of Physical Medicine andRehabilitation at the Mayo Clinic in Rochester, Minnesota. His researchinterests include spine biomechanics, the epidemiology of spine pathology,and lateral epicondylitis. In 2002, Dr. Brault was named Teacher of theYear in the Department of Physical Medicine and Rehabilitation.

Lyell K. Jones, MD

Chief

Electrodiagnostic Services

Wilford Hall Medical Center

Lackland Air Force Base

San Antonio, Texas

Dr. Jones completed his undergraduate and medical degrees at WakeForest University in Winston-Salem, North Carolina before going to theMayo Clinic in Rochester, Minnesota for his residency in neurology. Dr.Jones recently completed a fellowship in clinical neurophysiology at theMayo Clinic in Rochester, Minnesota, after which he joined the staff of theDepartment of Neurology at the Wilford Hall Medical Center at LacklandAir Force Base in San Antonio, Texas as their Chief of ElectrodiagnosticMedicine. His clinical interests include neuromuscular disease, and his aca-demic interests include resident education and the role of electrodiagnosisand neuroimaging in neuromuscular disease.

Keith Bengtson, MD

Assistant Professor

Department of Physical Medicine and Rehabilitation

Mayo Clinic College of Medicine

Rochester, Minnesota

Dr. Bengtson is currently a consultant and an assistant professor in theDepartment of Physical Medicine and Rehabilitation at the Mayo Clinicin Rochester, Minnesota. He earned his medical degree from theUniversity of Minnesota Medical School, performed a surgical internshipat Georgetown University, and went on to his residency in physical medi-cine and rehabilitation at Mayo Graduate School of Medicine. His clinicaland research interests include upper extremity pain syndromes and the careof instrumental musicians with upper extremity problems. Dr. Bengtson isa member of the American Academy of Physical Medicine andRehabilitation, the Performing Arts Medicine Association, the AmericanAssociation for Hand Surgery, and the Minnesota Physiatric Society.

Raza A. Awan, MD

Position

Department of Clinical Neurophysiology

St. Michael’s Hospital

Toronto, Ontario, Canada

Dr. Awan graduated from the University of Toronto Faculty of Medicineand completed his residency training in physical medicine and rehabilita-tion at the Mayo Clinic in Rochester, Minnesota. After completing hisphysiatry training, he performed an additional year of training in elec-tromyography and sports medicine at Mayo Clinic. Dr. Awan has com-pleted the American Board of Electrodiagnostic Medicine examinationand the Canadian Congress of Neurological Sciences EMG Certificationexamination. He has also completed the Canadian Academy of SportsMedicine Diploma in Sports Medication certification and holds a Mastersin Health Administration degree. He currently works in Toronto as aClinical Neurophysiologist at a teaching hospital and as a Sports MedicineDoctor at a private sports medicine clinic.

Course Chair: Andrea J. Boon, MD

The ideas and opinions expressed in this publication are solely those of the specific authors anddo not necessarily represent those of the AANEM.

Authors had nothing to disclose.

Please be aware that some of the medical devices or pharmaceuticals discussed in this handout may not be cleared by the FDA or cleared by the FDA for the spe-cific use described by the authors and are “off-label” (i.e., a use not described on the product’s label). “Off-label” devices or pharmaceuticals may be used if, in thejudgement of the treating physician, such use is medically indicated to treat a patient’s condition. Information regarding the FDA clearance status of a particulardevice or pharmaceutical may be obtained by reading the product’s package labeling, by contacting a sales representative or legal counsel of the manufacturer of thedevice or pharmaceutical, or by contacting the FDA at 1-800-638-2041.

iii

Painful Hip

Contents

Faculty ii

Objectives iii

Course Committee iv

Necessary Tools for Evaluation of the Painful Hip 1Jeffrey S. Brault, DO

The Painful Hip From a Neurologist’s Perspective 7Lyell K. Jones, MD

The Painful Hip From a Physiatrist’s Perspective 15Keith Bengtson, MD

Spotting the Zebra: Unusual and Challenging Cases 19Raza A. Awan, MD

CME Self-Assessment Test 23

Evaluation 27

Member Benefit Recommendations 29

Future Meeting Recommendations 31

O B J E C T I V E S —Hip pain is a commonly encountered presenting complaint in any neurologic or physiatric clinical practice. Afterattending this course, participants will (1) be familiar with the anatomy of the hip and pelvis, (2) understand key components of the his-tory and physical examination of the patient presenting with pain in the hip region, (3) understand the wide differential diagnosis of bothneurologic and musculoskeletal conditions that can result in a painful hip, including uncommon or controversial diagnoses such as thesportsman’s hernia, obturator nerve entrapment, snapping hip, impingement syndrome, and labral tears, and (4) develop a framework toevaluate and mange the painful hip, including appropriate use of laboratory testing, radiologic studies, and the role and limitations of theelectrodiagnostic evaluation.

P R E R E Q U I S I T E —This course is designed as an educational opportunity for residents, fellows, and practicing clinical EDX physiciansat an early point in their career, or for more senior EDX practitioners who are seeking a pragmatic review of basic clinical and EDX prin-ciples. It is open only to persons with an MD, DO, DVM, DDS, or foreign equivalent degree.

AC C R E D I TAT I O N S TAT E M E N T —The AANEM is accredited by the Accreditation Council for Continuing Medical Education toprovide continuing medical education (CME) for physicians.

CME C R E D I T —The AANEM designates attendance at this course for a maximum of 3.75 hours in category 1 credit towards theAMA Physician’s Recognition Award. This educational event is approved as an Accredited Group Learning Activity under Section 1 of theFramework of Continuing Professional Development (CPD) options for the Maintenance of Certification Program of the Royal Collegeof Physicians and Surgeons of Canada. Each physician should claim only those hours of credit he/she actually spent in the activity. TheAmerican Medical Association has determined that non-US licensed physicians who participate in this CME activity are eligible for AMAPMR category 1 credit. CME for this course is available 9/05 - 9/08.

iv

Thomas Hyatt Brannagan, III, MDNew York, New York

Timothy J. Doherty, MD, PhD, FRCPCLondon, Ontario, Canada

Kimberly S. Kenton, MDMaywood, Illinois

Dale J. Lange, MDNew York, New York

Subhadra Nori, MDBronx, New York

Jeremy M. Shefner, MD, PhDSyracuse, New York

T. Darrell Thomas, MDKnoxville, Tennessee

Bryan Tsao, MDShaker Heights, Ohio

2004-2005 AANEM PRESIDENT

Gary Goldberg, MDPittsburgh, Pennsylvania

2004-2005 AANEM COURSE COMMITTEE

Kathleen D. Kennelly, MD, PhDJacksonville, Florida

INTRODUCTION

The hip joint functionally transfers forces from the lowerextremity to the axial skeleton and vice versa. The hip is thelargest multiaxial ball joint, as well as the most stable joint inthe body, due to its osseus and ligamentous construction.There are many pathological processes that can mimic hippathology. Hip pain can be referred from the lumbar spine,sacroiliac joint, knees, and even the ankles. Most true intra-articular hip pathology becomes apparent during weight-bearing activities. It is imperative that hip pain be distin-guished from other causes by obtaining a comprehensive his-tory and physical examination.

APPLIED ANATOMY

The hip joint is a multiaxial ball-and-joint socket that main-tains its stability via its deep insertion of the head of thefemur into the acetabulum. The acetabulum is formed by thefusion of three pelvic bones, including the ilium, ischium,and pubis. This socket is deepened by the presence of alabrum around the rim of the acetabulum.

The stability of the hip is maintained through an extensivenetwork of very strong ligaments around the hip. Theiliofemoral ligament, also called the Y ligament or ligamentof Bigelow, is considered one of the strongest ligaments in the

body. It prevents hyperextension of the hip joint and isimportant in maintaining an upright posture. The pub-ofemoral ligament prevents excessive abduction of the femur(Figure 1A).

The femur and pelvis have extensive osseus componentsspecifically designed for muscular attachment. These compo-nents include the greater and lesser trochanters of the femurand the ischial tuberosity. The trochanters are sites of strongmuscle attachments and the ischial tuberosity serves as theprimary weight-bearing region when sitting. These osseouscomponents are protected by bursae including the trochanteric,ischiogluteal, and iliopectineal bursae (Figure 1B).

Musculature

Several muscles act upon the hip to provide motion. Thesemusculature complexes can be broken down into four pri-mary muscle groups. First, the flexor group or the anteriorquadrant consists of the iliopsoas muscle, which is the pri-mary hip flexor. This muscle also assists in hip external rota-tion. The sartorius muscle is a long strap-like muscle whoseprimary action is flexion of the hip, but also produces exter-nal rotation. The rectus femoris crosses both the hip and theknee joint, and acts as the flexor of the hip and the extensorof the knee. This is the only two-joint muscle of the quadri-ceps group. The tensor fascia lata (TFL) also serves as a weakhip flexor.

Necessary Tools for the Evaluation of the Painful Hip

Jeffrey Brault, DO

Assistant ProfessorDepartment of Physical Medicine and Rehabilitation

Mayo Clinic College of MedicineRochester, Minnesota

Secondly, the adductor group, which consists of five primarymuscles: the gracilis, pectineus, adductor longus, adductorbrevis, and adductor magnus. The adductor longus is themost superficial of this muscle group (Figure 2).

Thirdly, the abductor group, which consists primarily of thegluteus medius and minimus muscles. The gluteus medius isthe only palpable muscle on the lateral aspect of the hip(Figure 2).

Finally, the extensor group, which consists predominantly ofthe gluteus maximus, the primary hip extensor. The ham-string muscles consist of the biceps femoris, semitendinosus,and semimembranosus. These three muscles act as hip exten-sors and knee flexors. There are several muscles including thepiriformis, gemellus, and obturators, which function as mildhip extensors, but are fairly strong hip external rotators. Theyare deep to the extensor muscles and are intricately involvedin hip stabilization (Figure 2).

Innervation About the Hip

The neuronal supply about the hip is vast and beyond thescope of this manuscript. The components can be brokendown into either cutaneous, motor, or traversing nerves. Thecutaneous nerves consist of the ilioinguinal, genitofemoral,lateral femoral cutaneous, posterior femoral, perineal, andcutaneous branches of the dorsal rami. The large motor

branches are the femoral, obturator, superior/inferior gluteal,pudendal, and nerve-to-obturator internus. The major tra-versing structure is the sciatic nerve.

Blood Supply

The vascular supply to the hip and pelvis is supplied by thesuperior and inferior gluteal and pudendal arteries. The headof the femur receives vascular supply by the head of thefemoral artery and vein. These structures are susceptible toimpingement, resulting in avascular necrosis of the femoralhead.

DIFFERENTIAL DIAGNOSIS OF HIP PATHOLOGY

The differential diagnosis for hip region pain is broad.Superficially cutaneous and subcutaneous etiologies, such asrash, abrasions, contusions, and even herpes zoster, can resultin hip pain. Soft tissue infections and inflammation aroundthe hip, as well as intra-articular hip infections (septic jointand osteomyelitis), may result in hip region discomfort.Inflammation of the greater trochanteric bursa, ischial bursa,iliopsoas bursa, or obturator internus bursa can result in pain.

Musculotendinous etiologies of hip pain can result fromsprains of any of the muscles around the hip. Strains of theligaments surrounding the hip capsule, sacroiliac joint, or the

2 Necessary Tools for Evaluation of the Painful Hip AANEM Course

Figure 1

iliolumbar, sacrococcygeal, sacrospinous, or sacrotuberousligaments can result in pain. Other conditions, such asmyofascial pain syndrome or fibromyalgia can result in hipregion pain.

Spinal cord disorders, spinal stenosis, radiculopathy, plexopa-thy, and diabetic amyotrophy as well as peripheral neu-ropathies, which affect the sciatic, obturator, lateral femurcutaneous nerve (meralgia paresthetica) and ilioinguinal,congenital femoral, and pudendal nerve, may refer pain tothe hip region. Myopathies, such as muscular dystrophy, mayalso result in weakness and thus discomfort of the hip region.

Osteoarthritis, rheumatoid arthritis, psoriatic arthritis, andspondyloarthropathies of the hip joint proper or sacroiliacjoint may result in hip region pain. Gout and pseudogout arewell-known causes of intra-articular hip pain. Sacral, pelvicring, femoral, acetabular, or stress fractures are also common.Avascular necrosis, transient osteoporosis of the hip, which isthe result of irritation or compression of the vascular supplyof the hip, labral degeneration or tear, Legg-Calve-Perthes’disease, or slipped femoral capital epiphysis may cause hipregion pain. Neoplastic conditions, which can be metastaticto the hip region, include colorectal, pituitary, thyroid, blad-der, and renal.

Referred pain into the hip region can be the result of under-lying pathology of the bladder, uterus, cervix, vagina, ureter,testicle, penile, or colorectal region. Abdominal hernias canalso result in confusion with hip-region pain.

HIP EXAMINATION

History

Examination of the hip begins with a thorough patient history.Questions of particular interest are: What is the patient’s age?Usually the more degenerative conditions occur in people ofolder ages, compared to the congenital conditions such asLegg-Calves-Perthes’ disease, which occur most commonly inboys ages 3-12. Was any trauma involved or what was themechanism of injury? Did the patient land directly on theirhip, resulting in a trochanteric bursitis or was there an axialload which may be a resulting stress fracture? What is the cur-rent pain level? Where is the referral of pain? The patient canalso be asked to describe the pain, including the quality—isit burning, aching, and stabbing? Is there any snapping sen-sation? Is the condition improving, worsening, staying thesame? Are there any activities that make the pain worse orimprove it? Is weight-bearing a situation that actually makes

AANEM Course Painful Hip 3

Figure 2

the symptoms worse? Has the patient identified any activitiesthat improve their symptoms? Have they initiated any trial ofmedications or therapeutic intervention which may offersome benefit?

Evaluation

The initial evaluation of the hip begins with observations ofthe patient’s movements and gait pattern. Significant intra-articular hip pathology may result in antalgia on the affectedside. The patient limits the amount of weight-bearing andthe duration of weight-bearing on the symptomatic side. Thepatient’s movement and gait pattern may also demonstrate acompensated or uncompensated Trendelenburg gait. This isusually the result of weakness of the hip abductors. In thestanding position, the patient’s posture of the lumbar spineshould also be observed, as well as balance and distal strengthwhich can be assessed with heel- and toe-walking. Leg lengthinequality can also be assessed in the standing position, mon-itoring the relative height of the iliac crest, the anterior supe-rior iliac spine, posterior superior iliac spine, and the heightof the greater trochanters.

Hip Range of Motion

Active range of motion of the hips in the cardinal planes,which is considered normal include hip flexion to 120degrees. This is measured with a goniometer with the axisabout the hip joint and the proximal arm of the goniometerbisecting the torso, the lower arm bisecting the femur.Normal extension of the hip is 0-10 degrees. Adduction ofthe hip is generally around 30 degrees. Abduction is 45degrees. Internal rotation of the hip is considered normal if itis greater than 35 degrees. This is often tested with the hipflexed to 90 degrees. External rotation is also assessed in asimilar manner. Normal external rotation is about 45 degrees.Degenerative joint disease of the hip often results in early lossof internal rotation.

Manual Muscle Testing of Hip Musculature

Generally the manual muscle testing of the hip is performedon the major muscle groups as a unit. These include hip flex-ors, extensors, abductors, adductors, internal, and externalrotators. If weakness is identified, specific manual muscletesting can be performed to isolate specific muscles.

One important aspect of manual muscle testing is to look forasymmetry of the strength of the hip muscles. Major musclegroups, which are tested, include the iliopsoas, which isinnervated by the upper lumbar roots (psoas major is sup-plied directly via the ventral rami of L1 – L3, and iliacusreceives its nerve supply from the L2 and L3 roots, via thefemoral nerve). This tests the lumbar plexus as well as the

femoral nerve. Hip adductors are primarily innervated by theL2, L3 level via the obturator nerve. Hip abductors are sup-plied by the superior gluteal nerve and are typically L5, S1.When conducting a manual muscle examination, the patientlays on his or her side and attempts to abduct the hip. Thisposition can also be utilized to isolate the gluteus medius.Hip extensors are innervated by the sciatic and common per-oneal nerve. L5 - S1 are the predominant lumbar roots thatinnervate this region. The gluteus maximus and hamstringmuscles are the predominant hip extensor groups. There areseveral dermatomal patterns that can refer pain to the hip.These include regions from T10 down to L5—even S1 cancause pain about the hip.

TESTS TO IDENTIFY LOSS OF MOTION CAUSED BY TIGHTMUSCULATURE

There are certain ways to identify muscle length. The teststhat are used are listed below.

The Modified Thomas Test

The modified Thomas test assesses the length of the hip flex-or muscles. This test is performed with the patient sitting atthe edge of the table. The examiner brings one knee to thechest, where the patient holds it with his or her hands. Thepatient then lies back onto the table, producing a relativeposterior tilt with the pelvis. The examiner observes if thepatient is unable to fully extend the contralateral hip with theknee flexed to 90 degrees. This suggests a tight iliopsoas.

Determination of the Popliteal Angle

Hamstring tightness can be assessed by determining thepopliteal angle. To perform this test, the patient lies supine.The examiner passively flexes the hip and knee to 90 degrees.The patient’s lower limb is then passively straightened. Theexaminer maintains the hip at 90 degrees flexed position. Theangle between the upper and lower leg is then measured.There are no universally agreed upon normative values. Apositive test is identified by a finding of asymmetry of rightversus left.

Ober’s Test

The Ober’s test is utilized to assess tightness of the TFL andiliotibial band (ITB). In this test, the patient is side-lyingwith the test leg superior. The knee is slightly flexed. Theexaminer stabilizes the pelvis with the hand closest to thepatient’s head. The hand closest to the patient’s foot passive-ly flexes the hip, abducts the hip, and then extends the hip toend range, while not allowing the pelvis to move. The exam-iner then allows the hip to drop or adduct without losing


control of the pelvic tilt. A positive test is less than 15 degreesof hip adduction. This is secondary to ITB and TFL tight-ness. The primary indication of pathology is asymmetry ofthis test. It is imperative while performing this test that thepelvis is maintained in the same position on the table.

Ely’s Test

Ely’s test is utilized to test the tightness of the rectus femoris.In this test, the patient lies prone. The examiner passivelyflexes the knee and watches for the buttock to rise on oneside. This test is positive if there is asymmetry and the ipsilat-eral buttock rises fairly quickly. This suggests rectus femoristightness.

Piriformis Length Test

The piriformis length test can assess for piriformis syndrome.In this test, the patient lies supine. The hip is flexed to 90degrees, at which time the piriformis is considered an exter-nal rotator. The test ankle is placed on the outside of the con-tralateral knee, applying an axial force load along the femur,attempting to move the hip into internal rotation. At 90degrees of hip flexion, the piriformis then is converted into ahip internal rotator. A positive test results in tightness or painsuggestive of piriformis tightness. Again, it is important totest for asymmetry.

Special Tests of the Hip

Specific tests have been described to identify either intra-articular or peri-articular pain generators about the hip. Theirspecificity and sensitivities in identifying pathology vary sig-nificantly, but can assist in determining if the true cause ofpain is primarily hip or referred pain.

Hip Flexion Abduction and External Rotation

The hip flexion abduction and external rotation test is per-formed by having the patient lie supine. The hip is flexed and

the ankle is placed on the contralateral knee. The hip is thenallowed to extend, abduct, and externally rotate. Pain radiat-ing to the groin or about the hip region is considered a posi-tive test.

Stinchfield’s Test

The purpose of Stinchfield’s test is to provoke pain in the set-ting of intra-articular hip disease. In this test, the patient islying supine with the knee extended. The patient then liftstheir leg 30-50 degrees off the table. With the patient main-taining this position, the examiner resists further hip flexion.A positive test is indicated by groin pain. This is suggestive ofintra-articular hip pathology.

Anterior Labral Stress Test

The primary purpose of the anterior labral stress test is toprovoke pain that is the result of anterior labral tears or insta-bility. This test is performed with the patient in a supine posi-tion. The ipsilateral leg is dropped off the edge of a table. Theexaminer abducts and extends the hip and externally rotatesthe hip in an attempt to anteriorly displace the femoral head.A positive test is indicated if the patient describes groin painor a click is noted in the groin, suggestive of a labral tear.

Pound Test

The purpose of the pound test is to identify if there is any evi-dence of occult fractures within the lower extremity andpelvis. This test is performed with the patient supine. Theexaminer actually loads the hip in various degrees of hip flex-ion and abduction. If pain is produced in the groin or hipregion, it is reasonable to proceed with further radiographicevaluation.

Fulcrum Test

The fulcrum test is utilized to identify the presence offemoral stress fractures. In this test, the patient is placed


supine. The examiner supports the posterior thigh with his orher thigh. The contact point serves as a fulcrum. The exam-iner then tends to passively extend the distal leg. The positivetest is indicated with the deep thigh pain. This may also sug-gest an intra-articular hip pathology, as well as a potential forstress fracture.

CONCLUSION

Hip pain can be the result of hip-region dysfunction orreferred by surrounding structures. It is important to under-stand the anatomy of not only the hip, but also the lumbarspine and lower extremity. In identifying hip pain etiology, athorough history and physical examination must beobtained. Treatment of identified pathology can thus beemployed accordingly.

SUGGESTED READING

1. Cipriano JJ. Regional orthopaedic and neurological tests, 4th edition.Philadelphia: Lippincott-Williams &Wilkins; 2002. p 326-349.

2. Feinberg JH, Moley PJ. The physical examination. In: DeLisa JA,Gans BM, Walsh NE, Bockenek WL, Frontera WR, Geiringer SR,Gerber LH, Pease WS, editors. Physical medicine and rehabilitation:principles and practice, 4th edition. Philadelphia: Lippincott-Williams &Wilkins; 2004. p 49-60.

3. Hoppenfeld S. Physical examination of the spine and extremities.Norwalk: Prentice Hall; 1976. p 133-170.

4. Ganter BK, Erickson RP, Butters MA, Takata JH, Noll SF. Clinicalevaluation. In: DeLisa JA, Gans BM, Walsh NE, Bockenek WL,Frontera WR, Geiringer SR, Gerber LH, Pease WS, editors. Physicalmedicine and rehabilitation: principles and practice, 4th edition.Philadelphia: Lippincott-Williams &Wilkins; 2005. p 1-48.

5. Magee DJ. Orthopedic physical assessment, 4th edition.Philadelphia: WB Saunders; 2002. p 607-655.

6. McPeak JA. Physiatric history and examination. In: Braddom RL,editor. Physical medicine and rehabilitation. Philadelphia: WBSaunders; 1996. p 3-41.

7. Moore KL. Clinically oriented anatomy, 2nd edition. Baltimore:Williams & Wilkins; 1985. p 396-564.

8. Netter FH. Musculoskeletal system. In: The CIBA collection of med-ical illustrations, volume 8. West Caldwell: CIBA-GEIGY; 1987. p75-95.

9. Slaby FJ, McCune SK, Summers RW. Gross anatomy in the practiceof medicine. Malvern: Lea & Febiger; 1994. p 189-210.


The views expressed in this manuscript are those of the author and do notreflect the official policy or position of the United States Air Force,Department of Defense, or the United States Government.

INTRODUCTION

Pain is a common reason for patient self-referral for primaryand specialty care in the United States.7 While the burden ofpain is carried by the patient, it becomes the burden of theevaluating clinician to (1) evaluate carefully the patient’s clin-ical syndrome, (2) define the generator of the patient’s pain,and (3) develop a thoughtful treatment plan to manage thatpain.

As simple as it may seem, this process is fraught with perilfrom the first step. In an era with ample and readily-accessi-ble sources of medical information for the layperson, apatient’s personal investigation into his or her symptoms maybegin well before an initial visit to a health care provider.These diagnostic preconceptions may be shaped by thepatient’s underlying medical conditions (“My hip hurts…perhaps it’s my carpal tunnel”), disease states prevalent infriends or family (“My hip hurts… perhaps, like UncleRalph, I have the carpal tunnel”), or by the information avail-able on the internet, whose ubiquity is matched only by itsunreliability (“My hip hurts… and after 10 hours surfing theweb looking for an answer, I have the carpal tunnel”). If mis-informed, these preconceptions can cloud the clinical pictureconsiderably.

In the evaluation of the patient with the painful hip, partic-ularly among the self-referred, it is therefore crucial to sortout the precise spatial and temporal pattern of the patient’ssymptoms. This is particularly important among thesepatients, whose idea of what constitutes “hip pain” can varyconsiderably. True hip pain of strictly neurologic origin is rel-atively uncommon; however, patients who present for theevaluation of hip pain may commonly have a neurologiccause for some or all of their symptoms.

While hip pain may not be the most common manifestationof the entities discussed below, the open-minded clinicianmay uncover these diagnoses as potential contributors, andtherefore adapt the patient’s treatment plan accordingly.

LUMBOSACRAL RADICULOPATHIES

Clinical Features

Low back and lower extremity pain resulting from lum-bosacral radiculopathy is common.13 However, much as hippain is more commonly of musculoskeletal origin, isolatedlow back or isolated lower extremity pain is usually not neu-rogenic in nature.

That said, the classic pattern of lancinating, radiating pain inan anatomically correct dermatomal distribution is not a sen-sitive harbinger of lumbosacral radiculopathy. It is helpful

The Painful Hip From a Neurologist’s Perspective

Lyell K. Jones, Jr. MD, Captain, USAF, MC

Chief of Neuromuscular Disease ServicesDepartment of Neurology

Wilford Hall Medical Center, 59th Medical WingSan Antonio, TX

7

when this pattern declares itself to the clinician, ideally withmyotomal weakness and reflex loss as an accompaniment.More commonly, patients will complain of ill-defined unilat-eral or bilateral radiating pain which often occurs in a “skip”pattern. The onset of pain is often acute or subacute, thoughby the time the patient has reached the point of consultantevaluation, the pain has become chronic. Therefore, althoughthe neuromuscular clinician will be less likely to evaluatethose patients whose natural history is brief, he or she willoften have the advantage of an adequate duration of symp-toms for electrodiagnostic (EDX) testing to become useful(typically several weeks).

As alluded to in the introduction, a patient’s definition ofwhat constitutes the “hip” may vary. As such, in consideringpotential radicular causes for hip pain, the first step is toidentify where the patient’s “hip pain” really is. In patientswho identify the groin or inguinal fold as a locus of pain,higher lumbar radiculopathies (L2, L3, or less likely L4) maybe the culprit. Less commonly, patients will be referring totheir perineum or genitalia, and in such cases lower sacralradiculopathies (as may be seen in the cauda equina syn-drome and its additional clinical features) could be consid-ered. Patients who identify the lateral hip as the source ofpain may have L5 radiculopathies (once common entitiessuch as trochanteric bursitis have been considered). Finally,the modest patient who refers to the buttock as the “hip” mayhave an L5 or sacral radiculopathy. Always important torecall is the significant minority of patients who haveanatomic variation (the “prefixed” or “postfixed” lumbosacralplexus), in whom the precise level of radicular involvementmay vary.

The physical examination findings associated with lum-bosacral radiculopathies are well described, and a detaileddescription is beyond the scope of this manuscript. Suffice itto say, a neurologic examination in patients who present withthe painful hip is warranted. Any weakness identified, orreflex loss or asymmetry, particularly in a myotomal pattern,may alert the careful clinician to the presence of a lum-bosacral radiculopathy (Tables 1 and 2).

Electrodiagnostic Findings

Patients who present with a painful hip, who do not have his-torical features suggestive of lumbosacral radiculopathy or anabnormal neurologic examination, likely do not require anEDX evaluation. However, among those patients whose his-tory or examination is suggestive of an abnormal exami-naiton, electrodiagnosis may simultaneously confirm thepresence of disease, quantify its severity, and exclude othercoexistent neurogenic processes. Furthermore, in the fre-quent setting of vague or conflicting findings on history or

examination, electrodiagnosis may become crucial in thelocalization of denervation.

The sensitivity of electrodiagnosis, particularly of needle elec-tromyography (EMG), increases with time and progressionof denervation.3 Within several weeks following axonal loss,needle EMG should detect fibrillation potentials in musclesaffected by radiculopathy, with reduced numbers of motorunit action potentials (MUAPs) under voluntary control.Over months, reinnervation by axonal sprouting or regrowthwill reduce the numbers of fibrillation potentials in exchangefor higher-amplitude, longer-duration MUAPs. With theexamination of muscles innervated by different root levels,the specific root or roots involved may be identified. Needleexamination of lumbosacral paraspinal muscles help to con-firm the preganglionic localization of most radiculopathies,as do preserved sensory responses in the affected limb orlimbs. In many cases, low amplitude compound muscleaction potentials (CMAPs) may be seen. Other techniques,such as F-wave chronodispersion analysis and dermatomalsomatosensory evoked potentials (SEPs), have beendescribed.

Imaging

As with the EDX evaluation of patients with the painful hip,imaging studies performed blindly are more likely to providefalse-positives than useful diagnostic information.5 It isimportant to identify the patient’s syndrome prior to imagingthe lumbosacral spine, particularly if hip roentgenography ormore sophisticated pelvic imaging is more likely to be useful.

Modern imaging techniques are sensitive (perhaps too sensi-tive) in the detection of structural and degenerative causes oflumbosacral radiculopathy. For spinal imaging, magnetic res-onance imaging (MRI) has become the technique of choice,given its multiplanar capabilities and superb soft tissue reso-lution. However, it is important to recognize the high fre-quency of mild or moderate degenerative changes in the nor-mal, pain-free population; it is therefore critical to achievesome level of certainty regarding the patient’s pain generatorbefore invasive spinal procedures are pursued.

Conventional and computed tomography (CT) myelographyare often helpful in supplementing information obtained onthe MRI, and may be necessary in patients who need imag-ing but are intolerant of MRI or have a contraindication toundergoing the procedure.

Treatment

Management of lumbosacral radiculopathy is a topic unto itself;there are many good sources of discussion on the subject.1,2,11

8 The Painful Hip From a Neurologist’s Perspective AANEM Course

As a general principle, once the diagnosis of symptomaticlumbosacral radiculopathy has been established, more inva-sive therapies are warranted in the setting of refractory painor progressing neurologic deficit. Generally speaking, symp-tomatic management with medications, physical therapy, andpercutaneous procedures are preferred in the absence of acompelling need for surgical decompression.

LUMBOSACRAL PLEXOPATHIES

Clinical Features

Lumbosacral plexopathies are increasingly recognized as causesfor lower limb pain, anesthesia, weakness, and wasting; it is easyto imagine that affected patients may have, as a component of


Muscle L2 L3 L4 L5 S1 S2 S3 S4

Iliopsoas � �

Adductor Iongus � � �

Rectorus femoris � � �

Vastus lateralis � � �

Vastus medialis � � �

Gluteus medius �

Gluteus maximus �

Biceps femoris-short head �

Biceps femoris-long head �

Anterior tibialis � �

Perneus longus � �

Posterior tibialis �

Flexor digitorum longus �

Gastrocnemius �

Soleus �

Abductor hallucis � �

External and sphincter � � �

Table 1 Myotomal innervation of lower extremity muscles. A wide range of anatomic variation among normal patients excludes a strictinterpretation of this summary, which should only be used as a guideline.

Reflex L2 L3 L4 L5 S1

Patellar � � �

Adductor � � �

Ext. hamstring �

Achilles �

Table 2 Myotomal contributions to commonly-elicited lower extremity muscle stretch reflexes.

their symptoms, hip pain (Figures 1 and 2). It is in fact thiscombination of limb pain with loss of function that may sug-gest to the patient that their hip is the culprit. Unlike the pre-ceding discussion of lumbosacral radiculopathies, duringwhich a general assumption of degenerative cause wasimplied, lumbosacral plexopathies are manifold in their eti-ologies and it is therefore difficult to make blanket statementsregarding their evaluation and management.

Nonetheless, the same principles of careful clinical evaluationapply. The presence of lower limb anesthesia, paresthesia, orallodynia point to a neurogenic cause of the pain, and anysensory symptoms not easily ascribed to a single dermatomeshould raise the spectre of a plexopathy. Presentations mayrange from the acute (as in traumatic plexopathies), subacute(as in inflammatory plexopathies), or insidious (as may beseen with neoplastic plexopathies). Particularly in the lattertwo settings, when there is often no clear inciting event forthe symptoms, patients may implicate their “hip” as thesource of their troubles.

The increasing recognition of the proximal diabetic neu-ropathies (also known as diabetic amyotrophy, diabetic lum-bosacral radiculoplexus neuropathies, and a score of other

names) bears particular mention. Diabetic patients, who as apopulation are older and more likely to be burdened by med-ical comorbidity, are at increased risk of developing lum-bosacral plexopathies in a subacute fashion, owing to whatappears pathologically as a patchy, asymmetric microvasculitis.The estimated prevalence in the adult diabetic population isapproximately 4%, and is generally a monophasic illness withrecovery over a period of months.4

Any patient who presents with progressive pain, numbness,and weakness in a lower limb, particularly in the setting ofconstitutional symptoms such as weight loss, should be eval-uated for malignancy.

Electrodiagnostic Findings

The EDX evaluation is useful in the identification of lum-bosacral plexopathies for a number of reasons. The unsus-pecting clinician may request the evaluation with a suspicionfor lumbosacral radiculopathy; even the wary clinician maysuspect an abnormality in the plexus but be unable todemonstrate it with clinical findings of weakness in affectedmuscles (particularly large, proximal muscles that may haverelatively preserved strength despite significant denervation).


Figure 1 Schematic representation of the lumbar plexus. Itshould be recognized that its geographic proximity to the sacralplexus makes anatomic distinction somewhat arbitrary.

Figure 2 Schematic representation of the sacral plexus. It shouldbe recognized that its geographic proximity to the lumbar plexusmakes anatomic distinction somewhat arbitrary.

In this setting, needle EMG is extremely helpful in examin-ing these subclinically affected muscles; given an appropriateduration of symptoms, affected muscles may demonstratefibrillation potentials and reduced recruitment of long-dura-tion, high-amplitude MUAPs. In patients in whom the lesionis strictly in the lumbosacral plexus, the needle EMG exami-nation of lumbosacral paraspinal muscles is normal.However, particularly in plexopathies that are inflammatoryor traumatic in origin, the lumbosacral roots or dorsal pri-mary rami may be involved, and a high index of suspicionmust be maintained for a lesion within the plexus. In contrastto patients with lumbosacral radiculopathies, plexopathicpatients’ sensory nerve action potentials (SNAPs) are morelikely to be absent in the affected limb. It is worth remember-ing that sensory studies may be relatively preserved in an areaof spared sensation, and multiple sensory studies (sural,medial or lateral plantar, superficial peroneal, or saphenous)may be required for a satisfactory assessment, particularly inpatients with patchy lumbosacral plexopathies. Lower limbCMAPs may also be low amplitude or absent in affected dis-tributions.

Imaging

In the patient who has an inflammatory lumbosacral plex-opathy (particularly if they are older) it is not difficult toimagine a setting in which the EDX findings may not clear-ly point to a lesion in the plexus (given the higher likelihoodof an abnormal paraspinal EMG8 and sensory responseswhich may be low amplitude or absent in normal individu-als). In these cases, imaging of the lumbosacral plexus is cru-cial. As with lumbosacral radiculopathies, the outstandingsoft-tissue resolution of MRI makes it the most commonmodality in the assessment of the plexus. Findings may rangefrom a discrete mass within the plexus, to nonspecificenlargement and post-contrast enhancement of the plexus, toa completely normal appearing plexus. The imaging study ismost helpful when positive, as a normal result excludes onlya minority of potential etiologies.

Treatment

The treatment of lumbosacral plexopathies varies widely,according to the specific etiology. Inflammatory plexopathiesin which a specific underlying diagnosis cannot be reacheddespite extensive evaluation and even plexus biopsy might betreated empirically with corticosteroids or intravenousimmunoglobulin. Symptomatic pain management may be

achieved with a number of medications including tricyclicantidepressants and antiepileptics.

MONONEUROPATHIES

In contrast to patients with lumbosacral radiculopathies orplexopathies, patients who have proximal lower limbmononeuropathies may present with a syndrome very sugges-tive of localized hip pathology. These entities should there-fore remain in the differential diagnosis for any patient whosepain is associated with a cutaneous distribution of reduced orabnormal sensation, or whose musculoskeletal evaluation isunremarkable.

Lateral Femoral Cutaneous Neuropathy

Patients with lateral femoral cutaneous neuropathy (com-monly known as meralgia paresthetica) will typically com-plain of a burning or tingling lateral or anterior thigh pain.Sensory loss may accompany this in a similar distribution.The nerve, which arises directly from the anterior rami of L2and L3, is typically compromised at its passage under the lat-eral portion of the inguinal ligament en route to its area ofcutaneous innervation. Commonly, though not always,affected patients will have had a recent gain in weight or arepregnant;6,11 in patients with other mononeuropathies oratypical findings, a vasculitic or other inflammatory processmay be suspected. Electrodiagnostically, SNAPs may besought or cutaneous sensory-evoked potentials performed,but the technical difficulty in performing these studies (evenin normal subjects) makes this diagnosis a largely clinical one.Treatment is symptomatic, and symptoms may regress withcorrection of the underlying cause.

Medial and Anterior Femoral Cutaneous Neuropathies

The medial and anterior femoral cutaneous nerves are cuta-neous branches of the anterior division of the femoral nerve;they supply the anterior and medial thigh, and damage tothem may result in sensory disturbance in these areas. Theyare rarely disturbed in isolation, and will most commonly beaffected in association with a femoral neuropathy causingweakness in hip flexor muscles and knee extensors. NeedleEMG will typically show neurogenic changes in these mus-cles, and a unilaterally absent or low amplitude saphenousSNAP may be diagnostic (although this response may beabsent in normal subjects). Inasmuch as femoral neuropathies


are usually traumatic when occurring in isolation (as frompelvic hematomas or from surgical traction), these neu-ropathies rarely present a diagnostic dilemma. Treatment isdirected toward cause.

Obturator Neuropathy

Patients with isolated obturator neuropathies will most com-monly describe medial thigh or groin pain, and thereforecould reasonably be expected to mimic intra-articular hipsymptoms.9 Patients will less commonly describe weakness ofthigh adductors. As with femoral neuropathies, patients withobturator neuropathies will most often have had a recenttrauma or pelvic or hip surgery, and the cause is rarely a mys-tery. Electrodiagnostic evaluation is largely limited to needleEMG, which typically demonstrates fibrillation potentialsand large MUAPs in affected muscles. The prognosis in post-traumatic cases is generally good.9

Superior and Inferior Gluteal Neuropathies

Mononeuropathies affecting the superior or inferior glutealnerves are uncommon, but typically caused by trauma, oftenby intramuscular injection in the case of the superior glutealnerve. The superior gluteal nerve supplies the most powerfulabductors of the hip, and patients will typically present withweakness and a contralateral “hip drop” (Trendelenberg’ssign). Damage to the inferior gluteal nerve will cause weak-ness and atrophy of the only muscle it supplies, the gluteusmaximus; patients who have weakness of this muscle mayimplicate their hip as the location of their weakness, given thedifficulty they may have climbing stairs. In patients who areweak, the needle EMG will demonstrate denervation ofaffected muscles, and can precisely localize the nerve affectedand exclude other considerations (such as lumbosacralradiculopathies). Many patients will already have had pelvicimaging with MRI prior to visiting with a neuromuscularspecialist, and this may show increased T2 signal in affectedmuscles, suggestive of edema and denervation. Managementis usually supportive.

Piriformis Syndrome and Other Sciatic Neuropathies

Sciatic neuropathies, when significant enough to cause axon-al damage, should only rarely present with a painful hip,given the often profound leg weakness that results. However,there are many lesser degrees of sciatic nerve injury or irrita-tion, and a controversial entity known as piriformis syn-drome has arisen from this category. First proposed by

Yeoman in 1928,14 this putative cause of sciatica has been indispute ever since. The anatomic relationship between thesciatic nerve as it passes through its pelvic outlet under thepiriformis muscle is the presumed mechanism of compres-sion of the nerve, which is thought to be intermittent. Thistypically results in buttock or posterior thigh pain. In somecases, the muscle is found to be unilaterally hypertrophied onthe symptomatic side, and occasionally anatomic variationsof the sciatic nerve will complicate the picture.10 Patients willtypically have a normal neurologic examination and EDXevaluation, making buttock pain the primary feature of thisdisorder. The difficulty with diagnosis makes rigorous studyof the piriformis syndrome difficult, and there is an unfortu-nate lack of randomized, controlled, blinded data regardingits management. Surgically, the piriformis muscle is oftensacrificed given its minimal contribution to hip abduction.Percutaneous injections of the muscle are also employed.

Other Lower Limb Mononeuropathies

Lesions of the iliohypogastric, ilioinguinal, or genitofemoralnerves are among the less common mononeuropathies affect-ing the proximal lower limb. These are often traumatic(indeed, iatrogenic), and are mentioned here for the sake ofcompleteness.

HIP PAIN OF MUSCULAR ORIGIN

As anyone who has experienced a muscle cramp will attest,skeletal muscles are well-supplied with sensory innervation,and derangement of muscles from any of a number of causescan present with significant discomfort. The large muscles ofthe pelvic girdle and upper thigh are no exception to this, andpatients who present with a painful hip may have pathologyreferable to this.

Focal Myopathies

Isolated, focal myopathies are often the result of trauma, beit a discrete event or chronic, repeated trauma. Numerouscases of injection-related myopathies with associated contrac-tures have been reported, and these are often painful.12 Giventhe predilection of gluteal muscles for sites of intramuscularinjection, both illicit and medically directed, patients whopresent with hip pain may volunteer this information.Muscle pain related to myonecrosis may be seen followingblunt trauma or in gluteal compartment syndromes; neitherof these scenarios is likely to present a diagnostic mystery.


Cramps

Muscle cramps are an explosive, painful contraction of skele-tal muscle, often preceded by muscle shortening and fascicu-lations, and relieved by stretching and rubbing of the affect-ed muscles. Cramps are extraordinarily common, affectingmost normal subjects at some point, and are increased in fre-quency in a number of settings including electrolyte distur-bances, autoimmune disorders, and neuromuscular derange-ments. While in most people cramps occur in leg muscles(particularly in the posterior compartment), in a number ofdisease states they may occur elsewhere. Patients who havedenervation resulting in pelvic girdle muscles may occasion-ally experience cramps in them. Patients with autoantibodiesdirected against potassium channels may develop manifesta-tions of continuous muscle fiber activity, of whose clinicalphenotype cramps are a part, particularly in axial or upperlimb muscles. It is important, when considering these possi-bilities, to ensure the patient is describing muscular painfrom a true cramp, and not from muscle pain or shorteningof other origin (many patients will in fact use the terms“pain” and “cramp” interchangeably). Benign cramps oftenrespond to quinine or electrolyte supplementation.

Musculoskeletal Pain Resulting From Excessive CentralActivation

Stiff-man syndrome is an uncommon disorder associatedwith progressive muscular rigidity and associated spasms,most commonly and severely affecting axial muscles. Theprecise mechanism of the disorder is unclear, but the presencein some patients of autoantibodies to the glutamic aciddecarboxylase 65 (GAD-65) enzyme, which is required forthe synthesis of the central inhibitory neurotransmittergamma-amino-butyric acid (GABA), has raised the spectre ofan autoimmune mechanism. A significant minority ofpatients will present with limb symptoms, particularly in thelower extremity. Treatment is often frustrating, but GABA-ergic agents such as long-acting benzodiazepines andbaclofen have enjoyed some success.

Lower Limb Dystonias

Paroxysmal posturing of a lower limb resulting from a focaldystonia is often mistaken by patients for muscle cramps.While dystonias do not typically reflect peripheral nerve ormuscular pathology, repeated involuntary contractions ofmuscles may cause pain and focal hypertrophy. Admittedly,these latter symptoms are likely less common in the lowerextremities. Dystonia is common among patients withparkinsonism, who will often describe their spasms as musclecramps.

Spasticity

Spasticity resulting from upper motor neuron lesions oftenresults in muscular pain in the distribution of the affectedlimbs. Given the high incidence of secondary musculoskele-tal complications arising from limb spasticity, it is importantto recognize and distinguish muscle pain related to spasticityfrom other causes. Physical therapy, muscle relaxant medica-tions, and botulinum toxin therapy are all used in the man-agement of spasticity.

Myotonic Disorders

Although any of a number of myotonic disorders may causeclinical or electrical myotonia, only a minority are likely tohave myotonia or muscle stiffness as a prominent componentof the presenting complaint. Most notably, patients withmyotonia congenita are likely to complain of muscle painand stiffness, often involving gluteal muscles, which mayrespond to medication such as mexiletine or antiepilepticmedications once the diagnosis is established.

SUMMARY

By and large, hip pain is most commonly not neurologic inorigin. However, what is billed as hip pain may in fact bepain in a different location, and it is particularly important toclarify with the patient the exact distribution and timing ofthe symptoms. Radiographic and EDX studies may assist inthe detection of neurogenic disease, but their results must beinterpreted in the appropriate clinical context. The presenceof sensory disturbance, or any weakness not directly referableto the pain, should prompt the clinician to consider othercauses—peripheral or central. The potential morbidity asso-ciated with missed diagnoses underscores the importance ofperforming at least a focused neurologic examination inpatients who present with the painful hip.

REFERENCES

1. Abram SE. Treatment of lumbosacral radiculopathy with epiduralsteroids. Anesthesiology 1999;91:1937-1941.

2. Chiodo A, Haig AJ. Lumbosacral radiculopathies: conservativeapproaches to management. Phys Med Rehabil Clin N Am2002;13:609-621.

3. Daube JR. Clinical neurophysiology, 2nd edition. Oxford: OxfordUniv Press; 2002.

4. Dyck PJ, Thomas PK. Peripheral neuropathy, 4th edition.Philadelphia: WB Saunders; 2005.

5. Jensen MC, Brant-Zawadzki MN, Obuchowski N, Modic MT,Malkasian D, Ross JS. Magnetic resonance imaging of the lumbarspine in people without back pain. N Engl J Med 1994;331:69-73.


6. Massey EW. Sensory mononeuropathies. Semin Neurol1998;18:177-183.

7. McQuay HJ, Moore RA, Eccleston C, Morley S, Williams A.Systematic review of outpatient services for chronic pain control.Health Technol Assess 1997;1:1-135.

8. Nardin RA, Raynor EM, Rutkove SB. Fibrillations in lumbosacralparaspinal muscles of normal subjects. Muscle Nerve 1998;21:1347-1349.

9. Sorenson EJ, Chen JJ, Daube JR. Obturator neuropathy: causes andoutcome. Muscle Nerve 2002;25:605-607.

11. Spinner RJ, Thomas NM, Kline DG. Failure of surgical decompres-sion for a presumed case of piriformis syndrome. Case report. JNeurosurg 2001;94:652-654.

11. Storm PB, Chou D, Tamargo RJ. Surgical management of cervicaland lumbosacral radiculopathies: indications and outcomes. PhysMed Rehabil Clin N Am 2002;13:735-759.

11. Weber M, Diener HC, Voit T, Neuen-Jacob E. Focal myopathyinduced by chronic heroin injection is reversible. Muscle Nerve2000;23:274-277.

12. Woolf AD, Pfleger B. Burden of major musculoskeletal conditions.Bull World Health Organ. 2003;

13. Yeoman W. ßThe relationship of arthritis of the sacro-iliac joint tosciatica. Lancet 1928;ii:1119-1122.


INTRODUCTION

What do physicians do when they see a 65-year-old patientwith unilateral anterior or lateral thigh pain that is limitinghis/her ability to walk or stand? How does a physician differ-entiate between L3 through L5 lateral stenosis and muscu-loskeletal causes of hip pain? Greater than 50% of asympto-matic individuals over the age of 60 have significant magnet-ic resonance imaging (MRI) changes of spondylosis, discdegeneration, degenerative joint disease, or stenosis. In thissame population, 30% will have some radiographic evidenceof hip osteoarthritis (OA). In a population where bothpathologies are likely to be present in the same patient, howdo physicians determine the real pain generator? The follow-ing is a discussion of the common musculoskeletal etiologiesfor hip pain.

DIFFERENTIAL DIAGNOSIS

In patients over the age of 50, the vast majority of all muscu-loskeletal hip pain is either hip OA or one of the many typesof bursitis in the hip region. In patients under the age of 50,labral tears or tendinitis should be considered. All other eti-ologies would be considered “uncommon” and are discussedin the next section.

Hip Osteoarthritis

Osteoarthritis of the hip commonly presents as pain in thegroin area, sometimes radiating to the anterior thigh andknee, or less often to the buttock or low back. Symptoms aretypically worse with weight-bearing activities. Patients maycomplain of walking with a limp or have difficulty with nego-tiating stairs, taking them one at a time. As the disease pro-gresses, the patient will have more difficulty with hip flexionand internal or external rotation. This may cause discomfortor an inability to put on shoes and socks, cross the legs, or getin and out of a car. These mechanical difficulties are the clear-est symptoms that differentiate the symptoms of hip OA andthose of unilateral pseudoclaudication, particularly at the L2through L4 levels. However, both diseases should producesymptoms of unilateral thigh pain with weight-bearing activ-ities that is relieved almost immediately by sitting or lyingdown.

Bursitis

There are a large number of bursae in the hip region that maycause pain. The three trochanteric bursae include the gluteusminimus, subgluteus medius, and the subgluteus maximus(Figure 1). Of these, the sub gluteus medius is the largest andmost often symptomatic. Approximately half of all cases are

The Painful Hip Pain From a Physiatrist’s Perspective

Keith A. Bengtson, MD

Department of Physical Medicine and RehabilitationMayo Clinic FoundationRochester, Minnesota

15

associated with an initial trauma. Many of these patients havecalcifications in the bursa that are seen on plain radiographs.Female-to-male ratio is reported as between 2:1 to 4:1. Thefemale predominance may be due to womens’ wider pelvisand larger Q-angle (Figure 2) which place greater stress onthe hip abductor and external rotator muscles. Presumably,the bursae become irritated when they are exposed to unduefriction and stress. This may occur after direct trauma to thelateral hip or when a weak, tight muscle or tendon is pushedbeyond its normal limits—as in a middle-aged woman whobegins a new exercise program that includes walking or theuse of a stair machine.

Symptoms are usually limited to the lateral hip and the but-tock area and may extend to just below the lateral knee.Symptoms are worse with weight-bearing because thisrequires activation of hip abductors, particularly in one-legged weight bearing. Climbing stairs or standing from aseated position may also aggravate the symptoms. Typicallythe patient has pain when lying on the affected side, as thearea is often sensitive to direct pressure. However, the patient

may also note pain when lying on the unaffected side becausethe iliotibial band (ITB) is tented over the greater trochanterin this position.

As one may imagine, the symptoms of lower lumbar pseudo-claudication are quite similar to trochanteric bursitis as bothsets of patients may present with lateral hip pain on weight-bearing activities and pain that is relieved by sitting down.

PATHOPHYSIOLOGY, ANATOMY, HISTORY, AND SYMPTOMS

Physical Examination

The principle feature of the patient with hip OA is anantalgic gait. The weight-bearing phase of the gait is short-ened on the affected side. If the patient steps onto the affect-ed side they tend to overshift their weight, causing the trunkto lean in the direction of the hip OA. This produces a wad-dling affect reminiscent of a penguin and is called a compen-sated Trendelenburg gait.

16 The Painful Hip From a Physiatrist’s Perspective AANEM Course

Figure 1 Hip bursae

Hip passive range of motion (PROM) is limited, especially ininternal rotation, often with pain in extremes of motion. TheStinchfield’s sign is the classic sign for hip OA. In order toillicit this sign, the patient lies supine and flexes their hipwith the knee extended as the examiner resists with a down-ward pressure on the lower leg. This should reproduce thepatient’s groin and anterior thigh pain. Of course, anypathology of the iliopsoas muscle (tendinitis, strain, bursitis,or abscess) would also produce a positive Stinchfield’s test.Tenderness to palpation is not usually seen.

In trochanteric bursitis, the patient may also have an antalgicgait, but usually not a prominent compensatedTrendelenburg gait. Tenderness to palpation is the hallmarkof the examination with tenderness directly over the greatertrochanter and often all the way down the ITB to just below

the knee. Pain might also be reproduced with passive internalrotation of the hip and perhaps with resisted abduction.

IMAGING STUDIES

Plain radiographs should be sufficient for the diagnosis andtreatment planning of hip OA. Both anterioposterior and lat-eral views may be augmented by a frog leg view. Generally,joint space narrowing is easily seen at the superior-medialaspect of the hip. Subchondral sclerosis and joint space irreg-ularities should be evident. Severe sclerosis or collapse of thefemoral head would be indicative of avascular necrosis(AVN). The presence of AVN is confirmed by MRI or bonescintigraphy.

Imaging may not be particularly helpful in trochanteric bur-sitis. Although up to 50% of the cases may have calcificationof the bursal sac on plain films, this is not a diagnostic find-ing. Similarly, bone scintography may have a mild uptakeand the level of the greater trochanter and MRI may showincreased T2 signal in the bursal sac. However, these findings,although quite sensitive, are far from specific. Therefore, thediagnosis of hip bursitis depends much more heavily on thehistory and physical examination.

TREATMENT

Unfortunately, the treatment of hip OA is quite limited.Most would view the progression of the disease as aninevitable march toward total arthroplasty; however, thesepatients should certainly not be left without treatment.Simple analgesics and anti-inflammatory medication shouldbe tried if not otherwise contraindicated. Most importantly,a gait aid such as a simple cane should be suggested. A caneshould be used in the hand contralateral to the affected hip.This is the most efficient way to take weight off the affectedhip and hip stabilizer musculature (Figure 3) as described byBlount as early as 1956. In this figure, N is the force exertedby the foot on the floor. W is body weight. One assumes thatthe force of the cane on the floor is 1/6 body weight (W/6)and the cane is placed 30 cm from midline. Biomechanically,this will reduce the stress on the abductor muscle from 1.6times body weight (1.6 W) to 0.6 W. The force on the hipjoint is reduced from 2.4 W to 1.3 W. Therefore, a cane in


Figure 2 Q-Angle

the opposite hand eases the stress on the hip joint, but alsoon the muscles affected by trochanteric bursitis.

Strengthening of the hip stabilizers may be helpful for treat-ing hip OA, but is not supported in the literature (whereasstrengthening for knee OA is shown to be beneficial). If con-servative treatment fails to give adequate pain relief, then hiparthroplasty may be indicated.

Unlike the case of hip OA, the goal of conservative treatmentfor trochanteric bursitis is to cure the disease. In addition tocane use, the treating physician should prescribe stretching ofthe ITB and hip external rotators in order to lessen the stresson the bursae. Icing may help control inflammation andpain. Ideally, these should be taught to a patient by a physi-cal therapist. The therapist may then perform an ultrasoundon the ITB and hip external rotators to aid in stretching thesemuscle groups. The patient should be on a home program ofstretching and icing twice per day.

If no progress is seen after 3 to 4 weeks of stretching, icing,and ultrasound, the treating physician may consider localinjection of corticosteroids. The steroid is mixed with a localanesthetic and injected directly into the bursal sac and sur-rounding soft tissues. Rarely is surgery considered. Surgicaltreatments include excision of the bursa and ITB release.

CONCLUSION

So, how do physicians differentiate between unilateral lum-bar stenosis and musculoskeletal disorders of the hip? Sinceboth problems are prevalent in the elderly, it would not beunusual to see both in the same patient. Moreover, neurolog-ic weakness or dysfunction of the hip group muscles may pre-dispose the patient to hip OA or trochanteric bursitis. It canalso be postulated that an antalgic gait from an underlyingmusculoskeletal disorder may exacerbate stenosis of the lum-bar foramina. Therefore, determining the greatest pain gen-erator is essential. In general, hip disorders are easier to treatthan spinal disease. If hip OA is suspected, a simple strategyis to perform a diagnostic injection into the suspected hipjoint. A long-acting anesthetic is injected under fluoroscopicguidance and the patient is reexamined. If the patient reportsnearly complete pain relief and their gait is normalized, thenthe hip OA is the likely pain generator.

If trochanteric bursitis is suspected, it is worthwhile to treatthe apparent bursitis conservatively with physical therapeu-tics. If the symptoms are unabated, a trochanteric injectionfor both diagnostic and therapeutic reasons could be per-formed. If the patient has no relief from these measures, itmay be necessary to address the lumbar stenosis. Ideally, thepatient will demonstrate a clear positive or negative responseto treatment, thus indicating the underlying pain generatorand guide appropriate treatment.

SUGGESTED READING

1. Blount WP. Don’t throw away the cane. J Bone Joint SurgAm1956;38:695-708.

2. DeAngelis NA, Busconi BD. Assessment and differential diagnosis ofthe painful hip. Clin Orthop Relat Res 2003;406:11-18.

3. Ganz R, Parvizi J, Beck M, Leunig M, Notzli H, Siebenrock KA.Femoroacetabular impingement: a cause for osteoarthritis of the hip.Clin Orthop Relat Res 2003;417:112-120.

4. Harrison DM. Forces on the leg. Toronto: University of Toronto;2003. p. 1-6.

5. McCarthy JC, Lee JA. Arthroscopic intervention in early hip disease.Clin Orthop Relat Res 2004;429:157-162.

6. Newberg AH, Newman JS. Imaging the painful hip. Clin OrthopRelat Res 2003;406:19-28.

7. Shbeeb MI, Matteson EL. Trochanteric bursitis (greater trochanterpain syndrome). Mayo Clin Proc 1996;71:565-569.

8. Troum OM, Crues JV 3rd. The young adult with hip pain: diagno-sis and medical treatment, circa 2004. Clin Orthop Relat Res2004;418:9-17.

9. van Baar ME, Assendelft WJ, Dekker J, Oostendorp RA, Bijlsma JW.Effectiveness of exercise therapy in patients with osteoarthritis of thehip or knee. Arthritis Rheum 1999;42:1361-1369.

18 The Painful Hip From a Physiatrist’s Perspective AANEM Course

Figure 3 Cane biomechanics

INTRODUCTION

Hip pain carries a broad differential diagnosis, and identify-ing the precise cause of hip pain can be challenging given theproximity to a number of localized structures and internalorgans. Hip pain may be secondary to musculoskeletal con-ditions, nerve entrapments, urinary tract or renal pathology,gastrointestinal conditions, gynecological disease, testicularor ovarian pathology, or referred pain from the knee or lowback. Strains, tendinopathies, bursitis, and degenerative dis-ease are common causes of hip pain, however it is importantto keep less common, yet potentially disabling hip conditionsin mind when evaluating individuals with hip pain. Thismanuscript will review four less common causes of hip painwhich the electrodiagnostic medicine physician is likely toencounter.

SNAPPING HIP SYNDROME

Symptomatic snapping in the hip may occur for a number ofdifferent reasons. When evaluating an individual with a snap-ping hip, it is important for the clinician to determine thecause of snapping in order to provide effective managementand treatment. The symptomatic snapping hip can be catego-rized into external, internal, and intra-articular conditions.Patients presenting with a snapping hip may describe a sen-sation of snapping, cracking, popping, grinding, clicking, orin some cases may feel as if the hip is dislocating. Painlesssnapping in the hip is common in the general population;however symptomatic snapping hip with significant painappears to be more common in athletes or dancers.

Clinical Features

External Variety

Individuals with external snapping hip syndrome will typical-ly complain of symptoms on the lateral aspect of the hip.This condition is usually caused by the posterior aspect of theiliotibial band, or less commonly the anterior aspect of thegluteus maximus, snapping over the greater trochanter.7

Although this can occur with an associated painfultrochanteric bursitis, painless snapping is probably morecommon. The snap is typically palpable and may also beaudible. Patients can often demonstrate the snap with certainmaneuvers during the clinical evaluation. This conditionseems to be more common in dancers who may experiencesymptoms during certain positions, for instance when theirhip is turned out. The cause of external snapping hip is oftenmore obvious than internal or intra-articular causes. Manyindividuals feel as if the hip is dislocating, as the snapping canbe very dramatic.

Internal Variety

Internal snapping hip is most often associated with the iliop-soas tendon snapping over the lesser trochanter, oriliopectineal eminence.7 Symptoms are typically felt in theanterior groin as opposed to the lateral aspect of the hip. Thiscondition may also be painless, however can be associatedwith painful iliopsoas bursitis. The snapping may be lessobvious when compared with the external variety of snappinghip, and may be felt as a palpable impulse in the anterior

Spotting the Zebra: Unusual and Challenging Cases

Raza A. Awan, MD

Department of Physical Medicine and RehabilitationClinical Neurophysiology

University of TorontoToronto, Ontario

19

20 Spotting the Zebra: Unusual and Challenging Cases AANEM Course

groin. This condition is common in ballet dancers, however,it may also be seen in runners and track athletes.

Intra-articular Causes

A variety of lesions may produce intra-articular snapping,however loose bodies and labral tears are most commonlydescribed. Symptoms are typically described in the groin, andthe onset may be abrupt or possibly post-traumatic. It may bechallenging to differentiate intra-articular causes of snappingfrom the internal variety of the snapping hip syndrome. Thesymptoms with intra-articular causes may come on more rap-idly, are often worse with weight-bearing, and the examina-tion may show pain with hip motion, particularly internaland external rotation.

Investigations

Plain radiographs are often normal in patients with snappinghip, but they may show degenerative changes, loose bodies,or fractures. A computerized tomography scan may be help-ful to identify loose bodies or fractures; bone is less common-ly implicated as the cause of a symptomatic snapping hip.Magnetic resonance imaging is useful for the evaluation ofintra-articular causes of hip snapping such as labral tears,osteochondral fractures, or loose bodies, and can also be help-ful in visualizing bursitis which can be associated with symp-tomatic snapping hip. Static and dynamic ultrasonography isvery operator-dependent, but it may be helpful in demon-strating abnormal jerking of the tendon which may corre-spond to the patient’s painful sensation as well as the palpa-ble and audible snapping.3 An ultrasound examination mayalso demonstrate tendon thickening and bursitis in individu-als who have associated pain.

Treatment

Many cases of internal or external snapping hip syndrome arerelatively painless, and individuals may not even present forevaluation or treatment. Initial nonoperative management isoften attempted in internal or external snapping hip, and thismay include relative rest, activity modification, medication,and physical therapy. If there is an associated trochanteric oriliopsoas bursitis, a corticosteroid injection may be warrant-ed. Surgery is sometimes indicated for internal and externalsnapping hip syndrome, and the general goal is to lengthenor release the band of tissue in order to reduce snapping andpain.5 The treatment of intra-articular snapping depends onthe underlying cause, and surgery may be indicated for indi-viduals with large loose bodies or symptomatic labral tears.

TRANSIENT OSTEOPOROSIS OF THE HIP

Idiopathic transient osteoporosis of the hip (ITOH) is a rare,yet potentially debilitating condition. This condition seemsto be more common in active young and middle-agedadults—particularly males—as well as pregnant women intheir second and third trimester.

Clinical Features

The onset is typically acute with unilateral hip pain whichprogressively worsens. The pain is felt in the groin region, butcan radiate to the anteromedial thigh and medial knee. Thereare generally no symptoms noted below the knee. In mostcases no history of injury or trauma is described. The pain isgenerally worse with weight-bearing as well as motion of thehip, and is relieved by rest. The symptoms of pain peak atabout 4-8 weeks, and then generally improve over time. Thetime course for improvement can range from 6-10 months.The cause of this condition is unclear, however the mostcommonly accepted theory is that microvascular injury caus-es tissue ischemia, resulting in bone marrow edema and cellinjury.4 The physical examination generally shows an antalgicTrendelenburg gait, and pain with hip motion, particularlyinternal and external rotation.

Investigations

Radiograph imaging may be normal early on in this condi-tion; however at 4-8 weeks after symptom onset, diffuseosteopenia may be noted on radiographs. A bone scan may beabnormal earlier than radiographs, and the bone scan canalso be helpful in following symptom resolution. Magneticresonance imaging scans show a characteristic but nonspecif-ic abnormality of homogenous bone marrow edema.6 Mildchanges may be noted in adjacent acetabular bone, butprominent acetabular findings may warrant consideration ofan alternative diagnosis. The bone cortex is generally intact inITOH, as opposed to avascular necrosis where there is a sub-chondral defect, or in a malignant lesion with focal corticaldisruption.6 Distinguishing ITOH from avascular necrosiscan be difficult; however the presence of a focal subchondralfemoral head defect or a classic crescent sign would favoravascular necrosis over ITOH.6

Treatment

Idiopathic transient osteoporosis of the hip is generally man-aged supportively, as the natural history of the disorder showsa gradual resolution of symptoms. No specific treatment has


been shown to alter the course of the disease and treatment isprimarily supportive. Pain management, protected weight-bearing, analgesics, and nonsteroidal anti-inflammatorydrugs are helpful. Physiotherapy for gait retraining, gait aids,range of motion, and strengthening exercises may be warrant-ed. In more severe or refractory cases, a surgical referral forpossible core decompression may be considered.1

FEMORAL NECK STRESS FRACTURE

The repetitive stress of sports and exercise on bone can leadto a stress fracture. Most stress fractures are uncomplicatedand heal well, but some less common stress fractures such asa femoral neck stress fracture have a higher risk of nonunionor progression to complete fracture, and are therefore impor-tant to identify.

Clinical Features

Stress fractures often present in an individual who has had arecent change in activity. This may include an increase in thequantity or intensity of training, introduction of a new activ-ity, poor equipment, or change in training environment. Lowbone mineral density, dietary factors, menstrual irregularities,or biomechanical abnormalities may also predispose to stressfractures.2 Most individuals present with exercise relatedpain. Females seem to be more commonly affected thanmales. Symptoms are typically described in the groin region,but can radiate down the anteromedial thigh towards theknee. The onset of pain may be gradual or acute, and gener-ally worsens with exercise. Examination typically shows painwith hip motion and may show reduced hip range of motion.

Investigations

Radiographs may show callous formation, but can be normal.If the index of suspicion for a stress fracture is high, a bonescan can be a very sensitive test.

Treatment

Distraction fractures are present on the superior margin ofthe femoral neck and can progress to complete fracture ordisplacement and may require open reduction internal fixa-tion.2 Compression fractures generally affect the lower medi-al margin of the femoral neck and carry an increased risk ofavascular necrosis and nonunion.2 Many stress fractures canbe managed nonoperatively, and conservative treatmentincludes relative rest, protected weight-bearing, and a gradualresumption of weight-bearing activity over approximately 6-8 weeks. Biomechanical issues or other risk factors such astraining errors may also need to be addressed. In female

patients, a high index of suspicion for the female athlete triadshould be maintained. The triad is described asosteopenia/osteoporosis, disordered eating, and menstrualdysfunction, and can predispose to stress fractures.

SPORTS HERNIA

A sports hernia is described as a disruption to the inguinalcanal that is resistant to treatment, in the absence of a clini-cally detectable hernia. Sports hernias are seen most frequent-ly in individuals participating in sporting activities whichinvolve quick cutting or turning, such as soccer or hockey.

Clinical Features

The typical presentation is one of groin pain which is worsewith exercise. The onset may be abrupt or gradual. Thesymptoms are generally felt more proximal and internal incomparison with typical groin or adductor strains. This con-dition appears to be more common in males. The pain canradiate to the perineum, rectus, adductor muscles, testicles,or scrotum. The symptoms may be worse with valsalva,coughing, sneezing, sexual intercourse, or when performing asit-up.9 On examination, the maximum point of tendernessmay be felt in the pubic tubercle or posterior and lateral tothe inguinal canal.8 An obvious and palpable hernia is usual-ly not present. This condition may coexist with osteitis pubisand adductor tendinopathy, and is often resistant to treat-ment. Ilioinguinal or obturator neuropathies may mimic thiscondition, and stress fractures of the pelvis or hip should alsobe considered.

Pathophysiology

The anterior wall of the inguinal canal consists of the exter-nal oblique aponeurosis and the internal oblique muscle.9

The posterior wall is formed by the fascia transversalis, whichis reinforced by the conjoined tendon (the common tendoninsertion of the internal oblique and transversus, whichattaches to the pubic crest).9 The superficial inguinal ring liesanterior to the conjoined tendon.9 Operative findings aredescribed as disruption of the conjoined tendon, a torn exter-nal oblique aponeurosis causing dilatation of the superficialinguinal ring, a torn conjoined tendon, dehiscence betweenthe torn conjoined tendon and inguinal ligament, weakeningof the transversalis fascia with separation from the conjoinedtendon,5 tears in the internal oblique muscle,11 and an incip-ient direct inguinal hernia with an associated bulge in theposterior inguinal wall.10 It is postulated that a sports herniaoccurs because adductor action during sporting activity cre-ates shearing forces across the pubic symphysis that can stressthe posterior inguinal wall.5 Consequent repetitive stretching

22 Spotting the Zebra: Unusual and Challenging Cases AANEM Course

or sudden and intense force to the transversalis fascia and theinternal oblique can lead to separation from the inguinal lig-ament.5

Investigations

A sports hernia is more of a clinical diagnosis, but plain radi-ographs or a bone scan may be obtained to rule out condi-tions such as degenerative disease, stress fracture, or osteitispubis. Herniography has been described; however, this tech-nique is operator-dependent and is not widely available.8

Treatment

Initial treatment involves relative rest and functional rehabil-itation with a gradual return to activity. Core stability train-ing, stretches, and strengthening are mainstays of rehabilita-tive treatment. In many cases, conservative treatment maynot be helpful, and many individuals will eventually requiresurgery.

SUMMARY

When evaluating hip pain, it is important for the electrodi-agnostic physician to consider a broad differential diagnosis.Knowledge of uncommon causes of hip pain is helpful whenformulating a differential diagnosis, and in conjunction witha detailed history, physical examination and appropriateinvestigations, the cause of hip pain can be elucidated in themajority of patients. An accurate diagnosis and early treat-ment should help to limit overall pain and disability andimprove referring physician and patient satisfaction.

REFERENCES

1. Apel DM, Vince KG, Kingston S. Transient osteoporosis of the hip:a role for core decompression? Orthopedics 1994;17:629-632.

2. Brukner P, Bradshaw C, Bennell K. Managing common stress frac-tures: let risk level guide treatment. The Physician andSportsmedicine 1998;26:39-48.

3. Cardinal E, Buckwaltre KA, Capello WN, Duval N. US of the snap-ping iliopsoas tendon. Radiology 1996;198:521-522.

4. Guerra JJ, Steinberg ME. Distinguishing transient osteporosis fromavascular necrosis of the hip. J Bone Joint Surg Am 1995;77:616-624.

5. Hackney RG. The sports hernia: a cause of groin pain. Br J SportsMed 1993;27:58-62.

6. Harrington S, Smith J, Thompson J, Laskowski E. Idiopathic tran-sient osteoporosis: a hidden cause of hip pain. PhysicianSportsmedicine 2004;28:82-96 .

7. Idjadi J, Meislin R. Symptomatic snapping hip: targeted treatmentfor maximal pain relief. Physician Sportsmedicine 2004;32:25-31.

8. Johnson JD, Briner WW. Primary care of the sports hernia: recogniz-ing an often-overlooked cause of pain. Physician Sportsmedicine2005;33:35-39.

9. Kemp S, Batt, ME. The sports hernia: a common cause of groin pain.Physician Sportsmedicine 1998;26:36-46.

10. Malycha P, Lovell G. Inguinal surgery in athletes with chronic groinpain: the sportsman’s hernia. Austr N Z J Surg 1992;62:123-125.

11. Simonet WT, Saylor HL 3rd, Sim L. Abdominal wall muscle tears inhockey players. Int J Sports Med 1995;16:126-128.

12. Williams P, Foster ME. Gilmore’s groin – or is it? Br J Sports Med1995;29:206-208.

13. Zoltan DJ, Clancy WG Jr, Keene JS. A new operative approach tosnapping hip and refractory trochanteric bursitis in athletes. Am JSports Med 1986;14:201-204.

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