BACK PAIN/MULTIPLE SCLEROSIS
From the annual Family Practice Review, sponsored by the University of Minnesota Medical School, Minneapolis
| COMMON-SENSE APPROACH TO BACK PAIN —Joseph A. Wegner, MD, Partner, Physicians Neck and Back Clinics,
Roseville, MN
|
| First visit for back pain: critical; set guidelines; determine how to manage problem, then describe it; let patients decide
whether approach right philosophy for them; goal to avoid chronicity (develops in 10% to 15% of patients)
|
| History and physical examination: history—ask about location and duration of pain, mechanism of onset, character
of pain, associated neurologic problems (leg or arm symptoms), constitutional symptoms, previous surgery, and
previous injuries (document in third party claims); ask whether pain chronic or chronic-recurrent and about exposure to
low back pain disability; get occupational history; consider having patient fill out questionnaire prior to visit
|
 | Directed physical examination: inspection and observation of patient; range of motion (ROM) and straight leg-raising
tests; neurologic evaluation (particularly lower extremities and sensory and motor reflexes); special tests if pain stabbing
or pulsatile or if aneurysm suspected; prostate examination in older men; pelvic examination in women if pain
correlates with menstrual cycle
|
| Waddell (magnifying) signs: back pain with turning (trunk twisting); back pain with minimal axial compression of head;
cogwheel muscle weakness; nonanatomic sensory loss; nonanatomic areas of tenderness; significant discrepancies of
straight leg-raising test in supine and sitting positions; disproportionate groaning or giving way with light touch; deep
pain with superficial skin pinch; comment—presence of several positive Waddell signs means patient trying to magnify
how he or she feels to make point
|
| Helpful hint 1: make early decision as to ability to support patient (ie, do you really believe him or her?); base decision
on—history (sound reasonable?); examination (look reasonable?) imaging (correlate with history and examination?)
Waddell signs; be wary if purported problem does not look reasonable (may lead to endless work slips, narcotic renewals,
disability forms); once decision made, “stick to your guns”
|
| Problems with making back pain diagnosis: 85% of pain nonspecific; patients want to know “what’s wrong”;
physicians want to tell patients “what’s wrong” (sometimes they make something up); patients usually believe what they
are told; advice—do not immediately tell patients what is wrong; first try to categorize patients into “bad” and “not bad”
categories (based on cause, not pain)
|
| Helpful hint 2: be totally honest; never make up diagnosis; permissible to present theories; explain when imaging studies
(eg, x-rays, magnetic resonance imaging [MRI]) indicated and not indicated; strive for consistency in dealing with patients
|
| Therapeutic options: passive treatment—involves modalities in which something done to patient; includes heat, ultrasound,
massage, chiropractic manipulation, medications, injections, acupressure, bracelets, and whirlpools; good for
short-term pain relief; active treatment –– something done by patient to help self; surgery
|
| Wegner’s rules on treatment: rule 1—“if you are a hammer, the whole world is a tack”; etiology of back pain according
to therapist—physical therapists (pelvis out of whack; one leg longer than other); chiropractors (subluxation);
massage therapists (spasms and knots); rule 2—utilize AIM protocol (anti-inflammatory drugs, information, motion)
|
| Anti-inflammatory drugs: explain dosage and warn about side effects; tell patients to take agents (eg, ibuprofen,
naproxen) “just like antibiotics,” ie, for 10 days, then discontinue if no longer needed; information—provide packet
or other handout; talk about imaging, surgical options, natural history, and typical course (improvement); motion—
critical; more people move, better off they will be
|
| Helpful hint 3: strike a balance; allow patient to take it easy to let things heal, but also allow him or her to experience
some pain to maintain motion; give patient permission to hurt (never say, “if it hurts, don’t do it”); tell patient balance
may change hourly, daily, or weekly
|
| Helpful hint 4: hurt vs harm; when ordering patient to engage in certain activities, also say, “I recognize that you will
hurt,” but then add, “my job is to do what I think is best for you, and while I recognize that this activity is hurtful, I don’t
think it is harmful”; remarks—limiting activity does not lead to better outcome; remind patients if they hurt, motion is
“the best way to go”
|
| Talking with patients: “reassure, reassure, reassure” them they will improve (85% get better); discuss fear vs common
sense; advise them that imaging studies generally reserved for suspected “bad things”; reassure them most cases of severe
back pain not caused by something terrible, and, unlike chest or belly pain, treatment does not vary with cause;
comments—speaker uses narcotics to “keep the balance” (“if they can keep the balance without them, I don’t order
them”); reserve imaging studies for suspected “bad things”
|
| Returning to work: speaker tells patients to go back to work when he says it is safe, even if they hurt; going back to work
part of getting better
|
| Case of 49-yr-old lawyer: injures low back while playing basketball; over next 48 hr, develops severe pain and tingling
in right leg and foot; on physical examination, has slight list to left, right antalgic gait, decreased sensation in right lateral
calf and first web space, 3 out of 5 weakness in right great toe extension and ankle dorsiflexion; symptoms reproduced
on right straight leg raising; bowel and bladder history negative; anatomic diagnosis—L4-L5; remarks—physician
must know anatomy; L3-L4, L4-L5, and L5-S1 anatomic disorders account for most back problems; C4-C5, C5-C6, and
C6-C7 disorders account for most neck problems; if symptoms correlate with anatomic location, no need for imaging;
many expensive decisions (eg, imaging studies, referrals) made because physician not competent in clinical examination
|
| Acute disc syndrome: only 1 in 10 cases requires surgery; ≈50% of those with hard neurologic findings do not require
surgery if given chance to recover
|
| Extremity symptoms: often referred from back or neck, particularly in those patients who claim pain stops at knee (in
some cases below knee); resolve when back treated
|
| Disc problems: pain control required; indication for possible use of narcotics; important to get patients comfortable in
order to talk to them; injections sometimes required; some experts give injections without first obtaining MRI because
symptoms indicate anatomic location involved
|
| Indications for surgery: acute—classic cauda equina syndrome (characterized by saddle anesthesia and changes in
bowel and/or bladder habits); progressive neurologic deficit (suspect if patient has flaccid foot; MRI usually done);
subacute—progressive neurologic deficit (not static loss); L5-S1 injury (check for strength by having patient tiptoe across
room or attempt to raise toes); L4-L5 injury (assessed by evaluating heel walking or duck walking); intractable disabling leg
pain
|
| MULTIPLE SCLEROSIS (MS) UPDATE —Randall T. Schapiro, MD, Director, Schapiro Center for Multiple Sclerosis,
and Clinical Professor of Neurology, University of Minnesota Medical School, Minneapolis
|
| Pathophysiology: MS disease of immune system (in AIDS, immune system underactive; in MS, overactive); in MS,
white blood cells (WBC) recognize myelin as foreign and attack it; immune cells (eg, lymphocytes, macrophages,
plasma cells) cross blood-brain barrier, and series of reactions occur that damage central nervous system (CNS); integrin
adhesion molecule that helps immune cells get into CNS (treatments needed to prevent this, eg, anti-integrin antibody);
in MS, proinflammatory neurotoxic factors and protective factors out of balance
|
| MS also disease of myelin: in peripheral nervous system, myelin made by Schwann cells and in CNS, by oligodendroglial
cells; Schwann cells remake damaged myelin readily, but oligodendroglia do not perform significant resynthesis
of damaged myelin, so myelin damage in CNS permanent
|
| MS also disease of axons: myelin surrounds axons and makes nerve conduction more efficient; imaging techniques show
severing of axons leads to permanent loss of nerve function; axon damage must be stopped early
|
| MS also disease of people: usually develops in prime of life
|
| Prevalence: MS occurs more often in women than men (1.8 to 1 ratio); cuts across all racial groups, but occurs mainly in
white people; incidence higher in those of higher socioeconomic class and in those who reside at higher latitudes (probably
related to genetic makeup of people, rather than to climate)
|
| Diagnosis: criteria—1) onset usually in people 15 to 55 yr of age; 2) fluctuations in neurologic symptoms; 3) multiple
abnormalities within brain and spinal cord; comments—in past, MS not diagnosed with first attack because neurologic
examination still normal (therefore, diagnosis delayed); today, MRI can show change in water content of brain
associated with early-stage MS
|
| MRI: highly sensitive, but not specific; suspect MS if patient in target age group has scars in white matter next to ventricles;
if contrast material injected, one can see “hot” lesions and scars
|
| Evoked potentials: electrodes placed on head to stimulate brain; positive test (slowing of nerve conduction in optic nerve)
indicates problem
|
| Cerebrospinal fluid (CSF) analysis: involves electrophoresis of CSF to look for oligoclonal bands; not as sensitive, but
more specific for MS than MRI
|
| Prognosis: over two thirds of untreated people with MS still walking 20 yr after diagnosis, but some require cane (50%
require cane 15 yr after diagnosis); 60% of people get better (for some time) no matter what is done, then regress to mean
|
| Categories of MS: 80% of people start out with fluctuating course (relapsing-remitting disease); if untreated, 50% eventually
progress (secondary-progressive disease); 10% of people progress from beginning (primary-progressive disease);
5% begin with progressive MS, then develop relapsing disease (progressive-relapsing MS); prevalence of MS types at
any one time—55% have relapsing-remitting, 30% secondary-progressive, and 15% have other forms
|
| Treatment: involves 1) disease management; 2) symptom management (backbone of therapy), and 3) “person” management
(dealing with patient needs, psychologic issues, and other problems of chronic disease)
|
| Approved drugs for relapsing MS: interferon beta-1b (Betaseron), interferon beta-1a (Avonex, Rebif), and glatiramer
(Copaxone); initial studies suggest these drugs similar, but drugs not all alike; Rebif same drug as Avonex, but
Rebif stronger because more of it given; potency of Betaseron similar to that of Rebif; Copaxone injected daily, has
fewest side effects, and easiest to tolerate; Betaseron and Rebif strongest drugs, followed by Copaxone and Avonex;
CRABS of MS management—Copaxone, Rebif, Avonex, Betaseron, steroids, and symptom management\Q
|
| Natalizumab (Tysabri): antibody against integrin molecule; prevents immune cells from crossing into CNS; given once
monthly intravenously (IV); use discontinued after 3 cases of progressive multifocal leukoencephalopathy developed
among users
|
| Approach to management: 1) stabilize patients with active MS; 2) select drug that really works; 3) employ “Tom
Kelley theory” in MS management (put patient in position where he or she can succeed); 4) if prognosis poor (eg, frequent
attacks, heavy MRI burden, pyramidal tract involvement, ataxia, cognitive difficulties, progressing disability, spinal
cord problems), treat early and aggressively; 5) inquire about needle phobia and frequent travel; 6) probe for anxiety
and depression and manage accordingly; 7) seek patient input; 8) determine which drug fits patient best; 9) if patient has
progressive MS, use or add different drugs (eg, mitoxantrone [Novantrone]; may cause heart problems) to regimen; 10)
more aggressive treatments for refractory patients include bone marrow transplantation
|
| Other issues in MS patients: spasticity—send patient to physical therapist for exercise program (eg, ROM, stretching
exercises); restless legs also common in MS (sign of spasticity); several drugs helpful, but sometimes botulinum
toxin (Botox) or baclofen pump required for intrathecal administration of medication; disability—answer is mobility;
weakness—in MS, exercise does not increase strength if patient lacks nerve supply in brain and spinal cord, but without
exercise, disuse causes deconditioning; therefore, right exercise program important; studies under way with investigational
drug (4-aminopyridine [potassium channel blocker]) to allow demyelinated nerves to conduct more efficiently
(this drug associated with higher rate of seizures)
|
| Role of temperature: heat makes MS symptoms worse, whereas cooler weather makes them better
|
| Fatigue: most disabling symptom in MS; 5 types— 1) normal fatigue, 2) neuromuscular fatigue, 3) deconditioning, 4)
fatigue of depression, and 5) lassitude (most common; overwhelming tiredness); amantadine helps ≈30% of patients;
fluoxetine [Prozac] helps significant number, but modafinil [Provigil] best drug (off-label use); employ occupational
therapist to deal with activities of daily living and to teach patient about energy conservation
|
| Psychologic issues: MS patients vulnerable to exogenous depression (for having MS) and endogenous depression (associated
with neurochemical imbalance caused by MS); stress typically exacerbates symptoms
|
| Mobility issues: provide whatever devices necessary to keep people active; start devices early so patients stay mobile
|
| Bladder problems: some bladders in MS patients small and do not store urine (good drugs available for managing problem);
some bladders do not empty well (indication for catheterization); dyssynergic bladder treated pharmacologically;
for nocturia, consider use of antidiuretic hormone to “turn off” kidneys at night
|
Educational Objectives
| The goal of this program is to educate the listener about back pain and multiple sclerosis. After hearing and assimilating
this program, the clinician will be better able to:
|
| 1. Evaluate the patient who presents with back pain.
|
| 2. List the various therapeutic options (passive, active, and surgical) for treating back pain patients.
|
| 3. Describe the pathophysiology of multiple sclerosis (MS).
|
| 4. Diagnose and treat patients with MS.
|
| 5. Attend to various medical problems (eg, spasticity, weakness, heat intolerance, stress, immobility, depression,
bladder disorders) that are common in MS patients.
|
Discussed on This Program
Amantadine HCl [Symmetrel]
Aspirin (many trade names)
Baclofen [Kemstro, Lioresal, Lioresal Intrathecal]
Botulinum toxin type A [Botox, Botox Cosmetic]
Fampridine (4-aminopyridine; 4-AP) [Neurelan] (investigational)
Fluoxetine HCL [Prozac, Sarafem]
Glatiramer acetate [Copaxone]
Ibuprofen (several trade names)
Interferon beta-1a (recombinant) [Avonex, Rebif]
Interferon beta-1b [Betaseron]
Mitoxantrone HCl [Novantrone]
Modafinil [Provigil]
Naproxen [Aleve, Anaprox, Naprosyn, Naprelan]
Natalizumab [Antegren, Tysabri]
Suggested Reading
Assendelft WJ et al: Spinal manipulative therapy for low back pain: a metaanalysis of effectiveness relative to
other therapies. Ann Intern Med 138:871, 2003; Boal RW, Gillette RG: Central neuronal plasticity, low back pain,
and spinal manipulative therapy. J Manipulative Physiol Ther 27:314, 2004; Boswell MV et al: Epidural steroids in
the management of chronic spinal pain and radiculopathy. Pain Physician 6:319, 2003; Bronfort G et al: Efficacy
of spinal manipulation and mobilization for low back pain and neck pain: a systematic review and best evidence synthesis.
Spine J 4:335, 2004; Ehrlich GE: Back pain. J Rheumatol 67(Suppl):26, 2003; Filippini G et al: Corticosteroids
or ACTH for acute exacerbations of multiple sclerosis. Cochrane Database Syst Rev (4):CD001331, 2000;
Hagen KB et al: Bed rest for acute low-back pain sciatica. Cochrane Database Syst Rev (4):CD001254, 2004;
Henderson H: Acupuncture: evidence for its use in chronic low back pain. Br J Nurs 11:1395, 2002; Jarvik JG,
Deyo RA: Diagnostic evaluation of low back pain with emphasis on imaging. Ann Intern Med 137:586, 2002; Keeley
KA et al: Natalizumab for the treatment of multiple sclerosis and Crohn’s disease. Ann Pharmacother 39:1833,
2005; Kohlbeck FJ, Haldeman S: Medication-assisted spinal manipulation. Spine J 2:288, 2002; Kraft GH et
al: Multiple sclerosis: early prognostic guidelines. Arch Phys Med Rehabil 62:54, 198l; Lang AM: Botulinum toxin
type A therapy in chronic pain disorders. Arch Phys Med Rehabil 84(3 Suppl 1):S69, 2003; Litwiller SE et al:
Multiple sclerosis and the urologist. J Urol 161:743, 1999; Lutz GF et al: Looking back on back pain: trial and error
of diagnoses in the 20th century. Spine 28:1899, 2003; Poser CM: The pathogenesis of multiple sclerosis: a
commentary. Clin Neurol Neurosurg 102:191, 2000; Rainville J et al: Exercise as treatment for chronic low back
pain. Spine J 4:106, 2004; Rice GP et al: Interferon in relapsing-remitting multiple sclerosis. Cochrane Database
Syst Rev (4):CD002002, 2001; Ryan M, Piascik P: Providing pharmaceutical care to the multiple sclerosis patients.
J Am Pharm Assoc (Wash) 42:753, 2002; Schapiro RT: Managing symptoms of multiple sclerosis. Neurol
Clin 23:177, 2005; Schapiro RT: Pharmacologic options for the management of multiple sclerosis symptoms. Neurorehabil
Neural Repair 16:223, 2002; Steutjens EM et al: Occupational therapy for multiple sclerosis. Cochrane
Database Sys Rev (3):CD003608, 2003; Toth PP, Urtis J: Commonly used muscle relaxant therapies for acute low
back pain: a review of carisoprodol, cyclobenzaprine hydrochloride, and metaxalone. Clin Ther 26:1355, 2004; Van
der Roer N et al: What is the most cost-effective treatment fore patients with low back pain? A systemic review.
Best Pract Res Clin Rheumatol 19:671, 2005; Van Tulder MW et al: Muscle relaxants for nonspecific low back
pain. Cochrane Databases Syst Rev (2):CD004252, 2003; Zhang J et al: A comparison of the mechanisms of action
of interferon beta and glatiramer acetate in the treatment of multiple sclerosis. Clin Ther 24:1998, 2002.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial
relationship with the manufacturer or provider of any commercial product or service discussed. For this issue,
the faculty reported nothing to disclose.
Drs. Schapiro and Wegner were recorded May 4, 2006, in Minneapolis, MN, at the annual Family Medicine Review,
sponsored by the University of Minnesota Medical School, Minneapolis. The Audio-Digest Foundation thanks the
speakers and the medical school for making this program possible.
|
