ISSUES AND CONTROVERSIES IN THE INJURED WORKER€¦ · American Society for Clinical Investigation...

��American Association of Neuromuscular & Electrodiagnostic Medicine

Laurence J. Kinsella, MD

Asa J.Wilbourn, MD

ISSUES AND CONTROVERSIES

IN THE INJURED WORKER

2005 AANEM COURSE CAANEM 52ND Annual Scientific Meeting

Monterey, California

2005 COURSE CAANEM 52nd Annual Scientific Meeting

Monterey, California

Copyright © September 2005American Association of Neuromuscular & Electrodiagnostic Medicine

421 First Avenue SW, Suite 300 EastRochester, MN 55902

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Laurence J. Kinsella, MDAsa J.Wilbourn, MD

Issues and Controversies in the Injured Worker

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Faculty

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Nortin M. Hadler, MD*

Professor

Department of Medicine and Microbiology/Immunology

University of North Carolina

Durham, North Carolina

Dr. Hadler received his medical degree from the Harvard Medical School,and was trained at the Massachusetts General Hospital, the NationalInstitutes of Health, and the Clinical Research Centre in London beforejoining the faculty of the University of North Carolina where he isProfessor of Medicine and Microbiology/Immunology. He serves asAttending Rheumatologist at the University of North Carolina Hospitals.Dr. Hadler has authored over 200 papers and 12 books related to his spe-cial interest in the illness of work incapacity. He has lectured widely, gar-nered multiple awards, and served as a visiting professor in England,France, Israel, and Japan. He has been elected to membership in theAmerican Society for Clinical Investigation and the National Academy ofSocial Insurance. The third edition of his monograph OccupationalMusculoskeletal Disorders was published in 2005.

*Manuscript not included in the handout.


Professor of Neurology

Department of Neurology

Saint Louis University

Saint Louis, Missouri

Dr. Kinsella earned his medical degree from St. Louis University, complet-ed a neurology residency at Brown University/Rhode Island Hospital, anda neuromuscular fellowship at the Neurological Institute, Columbia-Presbyterian Hospital in New York. He currently is Chief in the Divisionof Neurology and Neurophysiology at Tenet-Forest Park Hospital in St.Louis, and is an associate professor of neurology at the St. Louis UniversitySchool of Medicine. Dr. Kinsella’s interests involve the clinical and electro-physiologic evaluation of patients with suspected peripheral neuropathies,especially those due to B12 deficiency and systemic medical illness.

Asa J. Wilbourn, MD

Director, EMG Laboratory

The Cleveland Clinic

Associate Professor

Department of Neurology

Case Western Reserve University

Cleveland, Ohio

Dr. Wilbourn received his neurology training at Yale University and hiselectrophysiology training at Mayo Clinic, Rochester, Minnesota. He is thedirector of the EMG Laboratory at the Cleveland Clinic, and is AssociateProfessor of Neurology at the Case Western Reserve University School ofMedicine in Cleveland. Dr. Wilbourn has extensively published on allaspects of the electrodiagnostic evaluation of plexopathies, radiculopathies,entrapment neuropathies, and iatrogenic nerve injuries. He has served as amember of the AANEM Education and Training Program Committees,and has been the chair of both the Membership and Progam Committees.Dr. Wilbourn has also served on the AANEM Board of Directors.

Course Chair: Alan R. Berger, MD

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

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Contents

Faculty ii

Objectives iii

Course Committee vi

Neurotoxicology in the Workplace: How to Evaluate Patients with Suspected Neurotoxic Peripheral Nerve Disease 1Laurence J. Kinsella, MD

The Role of EDX in Evaluating and Treating the Injured Worker 9Asa J. Wilbourn, MD

CME Self-Assessment Test 17

Evaluation 19

Member Benefit Recommendations 21

Future Meeting Recommendations 23

O B J E C T I V E S —Clinicians who specialize in neuromuscular disease are often asked to evaluate workers reportedly injured by their workactivities. After attending this course, participants will: (1) understand the current workers’ compensation and disability system and the roleit plays in the pathogenesis of workers’ symptoms, (2) appreciate the controversy surrounding the cumulative trauma theory to gain per-spective when evaluating symptomatic workers, (3) understand the difference between low back pain and the injured back, and how con-founding factors influence the pathogenesis, (4) understand the principles of neurotoxicology and develop a framework to evaluate whethera patient is suffering from neurotoxic peripheral nerve disease, and (5) understand the role and limitations of the electrodiagnostic evalua-tion of the symptomatic worker.

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 3.25 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.

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.

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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

IDENTIFICATION OF TOXIC PERIPHERAL NEUROPATHIES

Despite widespread media attention to their rare epidemicoccurrence, toxic polyneuropathies (TxPN) are relativelyinfrequent in North America. Most TxPN encountered inroutine clinical practice are due to iatrogenic pharmaceuticalintoxications; epidemic occupational exposure, as with largepharmaceutical companies, is unusual. The majority, andunfortunately the most difficult cases, of TxPN are individ-ual intoxications due to small scale, often chance occupation-al exposures, or intentional and homicidal ingestion.

The identification that a sporadic peripheral neuropathyresults from toxin exposure in the occupational setting isoften made difficult by an unclear exposure history. Toxicpolyneuropathies are usually distal axonopathies and clinical-ly and electrophysiologically resemble neuropathies frommetabolic abnormalities, nutritional deficiencies, or systemicillness. Clinically relevant and reliable toxicologic tests areoften unavailable or unhelpful, either because the necessarylaboratory tests are not available, or the substance is unde-tectable because of the delay between exposure and examina-tion. Consequently, when a naturally occurring medicalcause is not readily apparent, there is an unfortunate tenden-cy for many peripheral neuropathies to be misdiagnosed as

toxic in nature. As a result, cases of naturally occurring polyl-neuropathy are more often misdiagnosed as being toxic innature rather than the reverse.

The underlying pathology of many TxPN is the central-peripheral axonopathy. With continued exposure and wors-ening of the neuropathy, similar changes occur in the distalsegments of the dorsal column, and the corticospinal andspinocerebellar tract axons. Initial clinical symptoms reflectdysfunction in peripheral axons. As the peripheral nervesrecover, however, signs of central nervous system (CNS)impairment such as spasticity, mild ataxia, and persistent sen-sory loss may be evident. These latter deficits result from thelack of regeneration in central sensory and motor tracts.

Medicine’s limited knowledge of the biochemical and patho-physiologic mechanisms of most neurotoxins has led to asimplistic classification system according to compound class(e.g., solvents, metals). Such a classification is clinicallyunhelpful and potentially misleading. A compound cannotbe presumed to be neurotoxic because of a superficial resem-blance to a related known toxin of similar class; all com-pounds within the same class are not neurotoxic (e.g., acry-lamide monomer is capable of producing a devastatingperipheral neuropathy, while the polymer is innocuous).

Neurotoxicology in the Workplace:How to Evaluate Patients With Suspected

Neurotoxic Peripheral Nerve Disease


Professor of NeurologySaint Louis UniversityForest Park HospitalSaint Louis, MissouriAlan R. Berger, MD

Professor and Associate ChairmanDepartment of Neurology

University of Florida Health Science CenterJacksonville, Florida

Structure-toxicity relationships are clear for only a few class-es of substances, such as organophosphates and hydrocar-bons.

CARDINAL TENETS OF NEUROTOXIC ILLNESS AFFECTING THEPERIPHERAL NERVOUS SYSTEM

The identification of a neurotoxic illness should satisfy, or atleast not be inconsistent with, the following basic principalsof neurotoxic disease. The key to correctly recognizing thepresence of a TxPN is not in remembering the characteristicsof the many potential neurotoxins, but in understanding andapplying these basic tenets.

Strong Dose-Response Relationship

Most neurotoxins produce a consistent pattern of disease,commensurate with the dose and duration of exposure.Neurotoxins rarely cause focal or asymmetric deficits. Sincemost neurotoxins cause diffuse myelin and/or neuronal dys-function, their related symptoms and signs are usually wide-spread and symmetric. In the case of TxPN, this usuallymeans a relatively symmetric distal axonopathy with initialsymptoms in the feet and proximal progression, with contin-ued exposure. Only rarely does an occasional toxin causestrikingly asymmetric or focal dysfunction (e.g., trichloreth-ylene and cranial neuropathies).

Some patients with pre-existing neuropathy may experiencefar greater toxicity than expected for the dose received, asseen in patients with unsuspected Charcot-Marie-Tooth dis-ease who are exposed to chemotherapeutic agents.

Consistency of Response

All individuals with similar exposure to the same neurotoxinwill invariably manifest similar signs and symptoms (if thechemical enters the circulation, and if the agent, its metabo-lite or intermediate, has similar access to the nervous system).Although the same toxin may produce strikingly differentclinical syndromes if the exposure dose or duration is differ-ent, a similar and consistent illness should result in patientswith similar exposures. There is usually no individual suscep-tibility or idiosyncratic reactions if dose and duration ofexposure are similar. A neuropathy is unlikely to be neurotox-ic if it occurs in only one member of a group with similarexposure history. Likewise, neurotoxicity should also bedoubted when substantially different clinical manifestationsoccur in a group of individuals with identical chemical expo-sure.

Proximity of Symptoms to Exposure

Neurotoxic illness usually occurs concurrent with exposure orfollowing a short latency. Neurologic symptoms do not beginmonths to years after exposure. The two most commonexceptions are the 2-6 week delay following exposure toorganophosphates and the occasional 2 month latencybetween cisplatin intoxication and neuropathic symptoms.

In addition, the extent and severity of neuropathy is usuallycommensurate with the degree of toxin exposure. It is unlike-ly that a single, brief, low-level exposure will result in a dev-astating peripheral neuropathy. Some lipid stored agents(e.g., chlorinated hydrocarbons) are detectable in fat biopsiesyears following exposure. Although this provides a valuablemarker of previous exposure, there is no evidence that thisstate is associated with risk for future neurotoxicity, andattempts at removal or mobilizing the body burden areunnecessary.

Improvement Usually Follows Cessation of Exposure

Toxic polyneuropathies generally plateau and then graduallyimprove after removal of the neurotoxic agent. Some degreeof recovery is the rule, except in the most severely affectedcases. A neuropathy that shows no improvement or one thatcontinues to deteriorate despite the cessation of exposure to asuspected neurotoxin is unlikely to be neurotoxic in nature.However, the clinical picture may become somewhat murkyin certain toxic axonopathies in which cessation of exposuremay be followed by worsening of symptoms (coasting) forseveral weeks before recovery commences.

CONFUSING ASPECTS OF NEUROTOXIC ILLNESS

Multiple Clinical Syndromes May Result From DifferentLevels of Exposure to a Single Toxin

Different exposure levels to the same substance may producedramatically different syndromes. Most confusing is thebizarre constellation of symptoms that may arise from intox-ication with intermediate levels of the neurotoxin. Examplesinclude the different clinical syndromes produced by acutehigh-level and intermediate-level exposure, and prolongedlow-level acrylamide intoxication. Exposures to high-levelacrylamide causes early CNS dysfunction with drowsiness,disorientation, hallucinations, seizures, and severe truncalataxia, followed by neuropathy of variable severity.Prolonged, lower-level exposure causes little CNS dysfunc-tion but a marked peripheral neuropathy. Exposure to inter-

2 Neurotoxicology in the Workplace AANEM Course

mediate levels of acrylamide causes hallucinations, mentalconfusion, and cognitive dysfunction, followed by sensorycomplaints affecting the distal limbs.

Another example is organophosphate poisoning in whichthere may be early, severe cholinergic symptoms resultingfrom excessive muscarinic receptor stimulation. Within 1-3days there may occur generalized paralysis with respiratorydistress owing to nicotinic receptor blockade. After a fewweeks, a distal axonopathy may be evident.

In some instances, a single compound may produce similarclinical symptoms at both high- and low-level exposure,although different anatomic structures are affected. High-dose pyridoxine intoxication produces widespread sensoryloss due to dorsal root ganglion dysfunction; low-level expo-sure produces similar symptoms but is due to a distalaxonopathy.

Asymptomatic Disease

Prolonged, low-level exposure may occasionally producewidespread subclinical dysfunction. Clinical deficits may gounnoticed by the patient unless they perform an usuallyskilled job that requires fine-motor control or intact sensibil-ity. Insidiously developing subclinical TxPN may occur inindividuals who deny any disability.

Enhancement by Bystander Chemicals

An agent without known neurotoxic activity may enhancethe toxicity of a known neurotoxin that is present at a “noeffect” level. This disquieting notion has raised the public’sfear that the combined effects of multiple chemicals in haz-ardous waste disposal sites may be more toxic than their sep-arate effects. Such sites may contain low, presumably harm-less levels of neurotoxic solvents, metals, or pesticides, whoseneurotoxic potency conceivably might be enhanced by one ofthe other chemicals present. Neurotoxic potentiation is illus-trated by the epidemic of peripheral neuropathy whichoccurred in German youths who abused paint thinner con-taining n-hexane. Initially there were no instances of neu-ropathy, but when the paint thinner was reformulated bylowering the concentration of n-hexane and adding methylethyl ketone (MEK), there resulted an epidemic of severe dis-tal axonopathy. Experimental evidence subsequently showedthat while MEK by itself was not neurotoxic, the compounddramatically potentiated the neurotoxic effects of n-hexane.

Chemical Formula May Not Predict Toxicity

The neurotoxic potential of a compound cannot usually bepredicted by its chemical formula. This is especially impor-tant to consider when evaluating cases of potential occupa-

tional exposure to chemicals that superficially resemble aknown neurotoxin. An example is workers exposed to theinnocuous acrylamide polymer who have been needlesslyalarmed by physicians familiar only with the effects of acry-lamide monomer, a potent neurotoxin. Unpredictabilityexists because the underlying biochemical mechanisms andactive metabolites of most neurotoxins are unknown.

IDENTIFICATION OF TOXIC PERIPHERAL NEUROPATHY

The presence of a TxPN is suggested by the following:

a. suspicion raised by history and reinforced by com-patible findings on physical examination;

b. lack of naturally occurring alternative explanation;

c. consistency with basic principals of neurotoxic dis-ease;

d. compatible electrodiagnosis;

e. confirmation by demonstration of elevated bodyburdens if appropriate, or resolution of conditionwith removal of potential exposure.

The initial step is a suspicion raised by a thorough occupa-tional history. Unfortunately, because most TxPN are insidi-ous in onset, many patients are unable to discern a relation-ship between their symptoms and chronic, low-level, toxinintoxication. Inquiry should focus on potential occupational,environmental, and iatrogenic exposures. The individualhabits of a patient should be discussed. Does the patient wearprotective devices? Do they change their clothes before com-ing home? Do they eat in the workplace and wash their handsprior to eating? What is the health of their peers? Do symp-toms improve when they are away from the potential toxin,such as on weekends or holidays? Do workplace conditions(ventilation, drainage) predispose to an unacceptably highrisk of toxin exposure? Answers may only be available after avisit to the home or workplace itself. In cases of suspecteddomestic poisoning or substance abuse, home visits may beneeded to check hobby workshops, medicine cabinets, andfood and water sources. Inquiry should be made about recentpesticide applications. A similar illness found in a neighbormay prove helpful in identifying a neurotoxin.

The nature of the suspected toxin should focus the physicalexamination to relevant deficits. Thus a suspicion of mercu-ry poisoning should prompt a careful examination for tremorand mild cerebellar dysfunction. The function of the neuro-logic examination is to demonstrate that neurologic deficitsare in a pattern and of a severity that is consistent with

AANEM Course Issues and Controversies in the Injured Worker 3

neurotoxic illness. Since the clinical deficits resulting from aTxPN should be symmetric in distribution, the presence ofmultifocal deficits should suggest a diagnosis other than neu-rotoxic disease. In addition, since most TxPN affect mixednerve function, finding a purely small fiber neuropathymakes neurotoxic disease unlikely.

Occasionally the sensory or motor predominance of the neu-ropathic deficit gives some clue to etiology (Table 1).

Because of the heterogeneity of toxins and their often-unknown mechanisms of action, Schaumburg suggests a clin-ical classification based on cardinal manifestations of disease.Those agents with an A rating have a strong association witha particular clinical presentation, and a B rating is less strong(Tables 2-5).


Table 1 Clues to etiology

Motor Greater than Sensory Greater Than Motor Sensory Toxic Neuropathies Toxic Neuropathies

dapsone cisplatin

disulfuram pyridoxine

nitrofurantoin thalidomide

organophosphates thallium

lead arsenic

vincristine polychlorinated biphenyls

Table 2 Agents associated with peripheral neuropathy (Arating)

Acrylamide Ethylene oxide Organophosphates

Allyl chloride n-Hexane Phenol

Apamin & Hydralazine PyriminilHymenoptera

spp. venoms Hydrazine Thallium

Arsenic Karwinskia Vinyl chloridehumboldtiana

2-t-Butylazo-2-hydroxy- Lead Manihot esculenta

5-methylhexane Arsenic Methyl bromide

(reprinted with permission, Schaumburg51)

Table 3 Agents associated with peripheral neuropathy (Brating)

Carbamate pesticides Germanium dioxide

Chielanthes sieberi Mercury, inorganic

Ciguatoxin Methyl methacrylate

Dichloroacetic acid Tetrachloroethane

Euphoribia spp. “Spanish toxic oil”

Ethylene glycol

Table 4 Agents associated with neuromuscular transmissionsyndromes (A rating)

Black widow Fasciculins Pelamitoxinspider venom

Botulinum neurotoxin Hydrophiidae toxins Taipoxin

Carbamate pesticides Lophotoxin Trimethaphan

Ceruleotoxin Mamba snake toxin Erabutoxin

Cobra venom Mandaratoxin Organophosphorous

Crotoxin Methyllycaconitine compounds

Delphinium spp. Mojavetoxin Dendroaspisangusticeps

Ixodes holocyclus Dermocenter spp. Toxins

Table 5 Agents associated with axon ion channel syndromes (Arating)

Brevetoxins Kalmia latifolia Scorpion toxins

Buhotus hottentota Maitotoxin Tetrodotoxin

Ciguatoxin Pyrethroids Tityustoxin

Dichlorophenylethanes Saxitoxin Veratridine

Germine Ptychodiscus brevis

DETERMINATION OF BODY BURDENS

In the usual scenario, screening levels for heavy metals are notfruitful. Often this is because the toxin exposure was tooremote allowing time for the offending agent to be clearedfrom the serum. In some cases of prolonged exposures, likethallium or lead, finding elevated levels either in slow grow-ing tissues such as hair, or in urine or serum after chelation isoften diagnostic. In cases of prolonged exposure, the neuro-toxin may be sequestered in various tissues and thereforeunavailable for laboratory identification. With some chemi-cals, a safe level has not been established.

Serum lead levels greater than 30 mg/dL in adults and 10mcg/dL in children are toxic, but symptoms are most likelywith values greater than 80 mcg/dL. Free erythrocyte proto-porphyrin is a useful screening test in children. The assess-ment of body burden of lead requires chelation with ethylenediamene tetra acetate followed by a 24-hour urine collection.Values greater than 600 mg/24 hours are considered toxic.

Caution must be taken when interpreting body burdenresults. An example is arsenic levels. These are frequently oflittle clinical value and may be raised by recent shellfoodingestion. Total arsenic levels may include both inorganic(toxic) and organic (nontoxic form from shellfish ingestion)components. Arsenic levels greater than 50 mcg/L are abnor-mal, but patients with signs of toxicity usually have levelsgreater than 200 mcg/L. Twenty-four-hour urine collection ishelpful in those with elevated serum levels. Patients shouldabstain from shellfish for 3 days before measuring 24-hoururine or serum levels. The laboratory should separate resultsinto organic and inorganic forms to eliminate false positives.

ELECTRODIAGNOSTIC ASSESSMENT

Electrophysiologic findings should be consistent with a distalaxonopathy or mixed axonal, demyelinating neuropathy.Only a few rare neuropathies, such as n-hexane, perihexiline,amiodarone, and early arsenic poisoning, have predominantslowing of conduction velocities.

QUANTITATIVE SENSORY TESTING

Quantitative thresholds for thermal and vibration apprecia-tion have proven extremely useful in documenting objectiveevidence of sensory impairment and monitoring the courseof recovery or deterioration. These procedures are noninva-sive and reproducible and can be performed by a trainedtechnician. In an outbreak of arsenic poisoning, Kishi andcolleagues documented recovery of vibration perception

thresholds in survivors, whereas sural nerve responses showedno improvement. Berger demonstrated early abnormalities ofthermal and vibratory thresholds in subjects with normalclinical examinations who had been exposed to excessivepyridoxine (1-3 g/day).

SYSTEMIC FEATURES SUGGESTIVE OF NEUROTOXICDISEASE

The neuropathies resulting from most neurotoxins areremarkably similar in both their clinical and electrophysio-logic characteristics (Table 6). Occasionally, there may be sys-temic complaints or signs that suggest the nature of the neu-rotoxic insult. Usually these symptoms/signs are apparentwith either acute high-level, or chronic low-level intoxica-tion. The clinical characteristics listed in the Table 6 may bethe identifying feature that suggests a TxPN.


Table 6 Systemic signs and symptoms of occupational toxins

Toxin Systemic Signs and Symptoms

Acrylamide dermal contact associated with contact dermatitis, excessive sweating of hands and feet

Carbon disulfide chronic low-level exposure associated with a variety of behavioral and psychiatric abnormalities along with peripheral neuropathy

Ethyl oxide cognitive impairment and neuropathy with prolonged low-level exposure

Hexacarbons acute, high-level exposure may mimic AIDP with prominent autonomic dysfunction

Lead Mee’s lines, blood abnormalities (basophilic stippling, anemia), GI abnormalities, and predominantly a motor neuropathy

Mercury erythematous papulosis; tremor and ataxia with a predominantly sensory neuropathy

Methyl bromide corticospinal and cerebellar dysfunction along with an axonal neuropathy

Organophosphate early cholinergic symptoms, may have intermediate intoxication syndrome preceding neuropathy, late emergence of

corticospinal tract dysfunction as the peripheral neuropathy resolves

Polychlorinated symmetric sensory neuropathy associated with biphenyls brown acneiform skin eruption and brown

pigmented nails

Thallium prominent GI distress with high-level exposure, alopecia, Mee’s lines, hyperkeratosis with more prolonged exposure, sensory greater than motor neuropathy

AIDP = Acute idiopathic demyelinating polyneuropathy; GI = gastrointestinal.

Industrial workers and others may be exposed to a number ofknown neurotoxins. Table 3 lists the toxins, the occupationsand clinical signs, aids in diagnosis and treatment, and prog-nosis. What little may be known about the pathophysiologyis included.

Chinese herbal balls have been found to have potentiallytoxic levels of arsenic and mercury. They are a mixture ofmedicinal herbs and honey and are dissolved and drunk as atea. Mercury content in the 32 balls tested varied between 7.8and 621.3 mg per ball; arsenic content varied between 0.1and 36.6 mg. Chronic poisoning has been reported in peopleingesting as little as 10 mg per day of arsenic sulfide andamong people ingesting approximately 260 mg per day ofmercury sulfide.

SUMMARY

In summary, toxic neuropathies may occur from a variety ofsubstances in the workplace and in the home, but remainrare. Often the physician is faced with the difficult task ofruling out toxic etiologies in patients who suspect they havebeen poisoned. A careful exposure history, and an examina-tion consistent with known clinical patterns of injury aremost important in reaching a diagnosis.

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36. Kinsella LJ, Berger A, Harati Y, Kula R, Sivac M, Teitel L. Toxic,nutritional, and drug-induced neuropathies: a guide to the peripher-al neuropathies. New York, NY: The Neuropathy Association; 1998.

37. Kishi Y, Sasaki H, Yamasaki H, Ogawa K, Nishi M, Nanjo K. An epi-demic of arsenic neuropathy from a spiked curry. Neurology2001;56:1417-1418.

38. Korobkin R, Asbury AK, Sumner AJ, Nielsen SL. Glue-sniffing neu-ropathy. Arch Neurol 1975;32:158-162.

39. Le Quesne PM. Neurophysiological investigation of subclinical andminimal toxic neuropathies. Muscle Nerve 1978;1:392-395.

40. LeWitt P. The neurotoxicity of the rat poison vacor. A clinical studyof 12 cases. N Engl J Med 1980;302:73-77.

41. LoPachin RM, Lehning EJ. Acrylamide induced distal axon degener-ation: A proposed mechanism of action. Neurotoxicology1994;15:247-259.

42. Lotti M. Low-level exposure to organophosphorous esters andperipheral nerve function. Muscle Nerve 2002;25:492.

43. Lotti M, Becker CE, Aminoff MJ. Organophosphate polyneuropa-thy: pathogenesis and prevention. Neurology 1984;34:658-652.

44. Maurissen JP, Weiss B, Cox C. Vibration sensitivity recovery after asecond course of acrylamide intoxication. Fundam Appl Toxicol1990;15:93-98.

45. Murai Y, Kuroiwa Y. Peripheral neuropathy in chlorobiphenyl poi-soning. Neurology 1971;21:1173-1176.

46. Ohnishi A, Yamamoto T, Murai Y, Hayashida Y, Hori H, Tanaka I.Propylene oxide causes central-peripheral distal axonopathy in rats.Arch Environ Health 1988;43:353-356.

47. Osterman J, Zmyslinski RW, Hopkins CB, Cartee W, Lin T, NankinHR. Full recovery from severe orthostatic hypotension after Vacorrodenticide ingestion. Arch Intern Med 1981;141:1505-1507.

48. Risk Assessment Information System Website. August 9, 2004.Available at: http://risk.lsd.ornl.gov/. Accessed June 13, 2005.

49. Rollins YD, Filley CM, McNutt JT, Chahal S, Kleinschmidt-DeMasters BK. Fulminant ascending paralysis as a delayed sequela ofdiethylene glycol (Sterno) ingestion. Neurology 2002;59:1460-1463.

50. Saper RB, Kales SN, Paquin J, Burns MJ, Eisenberg DM, Davis RB,Phillips RS. Heavy metal content of Ayurvedic herbal medicine prod-ucts. JAMA 2004;292:2868-2873.

51. Schaumburg H. Neurotoxicology: human neurotoxic disease—occu-pational and environmental agents. Presented at: Meeting of theAmerican Academy of Neurology; April 9-16, 2005; Miami Beach,Fl.

52. Schaumburg HH, Spencer PS. Clinical and experimental studies ofdistal axonopathy: a frequent form of nerve and brain damage pro-duced by environmental chemical hazards. Ann NY Acad Sci1979;329:14.

53. Schaumburg HH, Spencer PS. Recognizing neurotoxic disease.Neurology 1987;37:276-278.

54. Schaumburg HH, Spencer PS. Selected outbreaks of neurotoxic dis-ease. In: Experimental and clinical neurotoxicology. Baltimore:Williams & Wilkins; 1980. p 883.

55. Schnorf H, Taurarii M, Cundy T. Ciguatera fish poisoning: a double-blind randomized trial of mannitol therapy. Neurology 2002;58:873-880.

56. Seppalainen AM, Tolonen M. Neurotoxicity of long-term exposureto carbon disulfide in the viscose rayon industry. A neurophysiologicstudy. Work Environ Health 1974;11:145.

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8 AANEM Course

INTRODUCTION

A long history is shared between the electrodiagnostic (EDX)examination and employees who have possibly sustainedwork-related peripheral nervous system (PNS) injuries.Electrodiagnosis generally is considered to have expandedfrom being solely a research tool to having clinical utility aswell with the 1943 publication of Weddell, Feinstein, andPattle’s article called “The Clinical Application ofElectromyography.”26 In 1950 and 1951, Woods and col-leagues described the method currently used for identifyingradiculopathies by the EDX examination.22,34 The fledglingdiagnostic procedure took a large stride forward when motornerve conduction studies (NCSs) were added to it in themid-1950s, after techniques for assessing some motor fibersof all the major peripheral nerves were described by Hodesand colleagues in 1948.11 In 1956, Simpson reported usingmotor NCSs to detect entrapment neuropathies of the medi-an nerve at the wrist, i.e., carpal tunnel syndrome (CTS), theulnar nerve at the elbow, and the ulnar nerve in the hand.23

This was a major advancement, because focal nerve lesionsmanifesting only demyelination could now be identified withmotor NCSs, thereby adding a new dimension to the EDXexamination (which, heretofore, using needle EMG alone,had essentially been restricted to detecting axon loss lesions).

One of the first articles to discuss the use of the EDX exam-ination in assessing patients with possible work-related PNSinjuries was Marinacci’s “The Electromyogram in IndustrialMedicine.”15 Published in 1954, it was surprisingly modernin its content, as judged by current standards. In regard to theEDX examination, it contained the following: criteria usedfor identifying nerve injuries; a method for distinguishingnerve injuries from psychogenic disorders; a procedure forrecognizing a radiculopathy and nine reasons why this wasbeneficial with possible root lesions; and points regarding itsusefulness in distinguishing changes, such as disuse atrophyof muscle or neurogenic findings caused by neuralgic amy-otrophy, from abnormalities resulting from actual work-relat-ed PNS injuries.15 A notable omission was the lack of com-ments regarding CTS. However, it must be remembered thatMarinacci’s article appeared in 1954, only 1 year after theclinical description of CTS was published by Kremer and col-leagues,14 and 2 years before Simpson’s report recounted theuse of motor NCSs for diagnosing CTS.23

In all industrialized countries, work-related injuries areresponsible for an enormous amount of disability, expense,and lost production. The single most common symptomassociated with such injuries is pain (less often, paresthesias),and the majority of these most likely are due to actual or

9

The Role of the ElectrodiagnosticExamination in the Evaluation and

Treatment of the Injured Worker

Asa J. Wilbourn, MD

Director, EMG LaboratoryCleveland ClinicCleveland, Ohio

alleged PNS or musculoskeletal disorders. Carpal tunnel syn-drome, as well as back, neck, and limb complaints, areresponsible for a considerable number of claims. Noteworthyis that limb pains, particularly when they involve the lowerextremity, are much more likely to be due to musculoskeletalcauses as opposed to neurological problems (e.g., root com-pression).19

In any case, many persons with presumed work-relatedinjuries are referred for EDX evaluations. Generally, the lat-ter are obtained only under certain circumstances: (1) if thediagnosis is not clear after a detailed history has beenobtained and a comprehensive physical examination has beenperformed; (2) if the results of the EDX examination wouldchange the management of the patient in some fashion; or(3) if they are needed for medical-legal reasons.7 Many factorsare involved in workplace injuries, not only occupational, butalso medical, psycho-social, and legal. These cases often dif-fer from similar ones that occur in the nonwork-related situ-ations, in that patients frequently have incentives to fabricateor exaggerate symptoms. Moreover, they often “present witha complicated mixture of symptoms resulting from recentinjury and exacerbation of pre-existing pathology.”16

Clinicians who examine patients with work-related injuriesare not only responsible for diagnosing and appropriatelytreating them, but also for determining their cause, establish-ing a causal relationship between the worker’s complaint andthe injury, and determining the degree of worker impair-ment.19 Moreover, the occupational physician is under con-siderable pressure to accurately diagnose and treat the injuredworker promptly, because returning him/her to work is theprimary goal, since there is compelling evidence that a majorbarrier to persons returning to work in these situations is theamount of time they have already been away from work dueto their injuries.3,25 Unfortunately, the treating physician canencounter a considerable number of impediments while try-ing to achieve these goals, beyond the problems posed by thePNS or musculoskeletal abnormalities that directly resultfrom the injury itself. These may be financial, psychological,or administrative in nature.

At least two financial disincentives can be encountered. First,the injured worker may be receiving a portion of their salarywhile not working. The amount received varies, but can besubstantial—up to 70% of normal earnings. While the logicfor this arrangement is obvious (i.e., to prevent financialhardship for the worker and his family), the practice oftenacts as a major deterrent to the worker returning to work,particularly if there are associated psychological factors.Second, sometimes the potential exists for the employee toobtain significant monetary gain via litigation. This is espe-cially likely to occur in situations where the worker has sus-tained a past injury and received a favorable settlement for it.

In this situation, the worker has strong motivation for notreturning to work because his/her absence strengthens theargument that substantial personal injury has occurred (and,therefore, a higher monetary settlement is in order).8

Psychological factors are often prominent. Many of these aredirectly work-related, such as job satisfaction related to non-challenging, or repetitive work, being a new employee, andstrained relationships between the employee and employer.8

Thus, Bigos and colleagues noted that a recent (preceding 6months) poor employee job performance evaluation was amajor psychologic factor that impeded the return to work ofemployees with low back injuries.4 The psychological factorsalso can impact the injured employee’s nonwork environ-ment. Stress and turmoil within the family can develop ifinjured workers relinquish social responsibilities that theyhave in their homes, even though they could perform themdespite their impairments. Moreover, some workers use theirinjuries as control factors to manipulate family members. Inaddition, some of them have underlying psychiatric disorderssuch as depression, which manifest under the circumstancesand impede their return to work.8

There are psychological issues pertaining to diagnostic testingthat may have a negative impact on return to work. Excessivediagnostic testing may increase the risk of false-positive stud-ies, thereby creating the impression that patients have moreprofound illnesses. It may also result in incorrect diagnoses.Thus, obtaining an excessive number of spinal imaging pro-cedures on patients with low back pain may lead to misdiag-nosis, since a co-existing but unrelated imaging abnormalitymay be considered the cause for the patient’s current symp-toms. This can create psychological stress for patients andtheir families and encourage those litigious workers to filelawsuits. In both instances, return to work is delayed.8

There are administrative factors that can thwart the occupa-tional physician’s goal of promptly returning the worker tohis employment. These may be both system-wide or relatedto a specific employer. Many workers are covered by thestate’s Worker’s Compensation system. Although these varyconsiderably from state to state, they all have one thing incommon—they are complicated.19 Often delays are encoun-tered before proper authorization can be obtained for proce-dures to be performed that the physician considers necessary(including EDX examinations). Under the Worker’sCompensation system, physicians usually are authorized totreat only the work-related injury.8 In regard to EDX exami-nations, that means only the symptomatic limb can beassessed (i.e., no studies can be performed on the contralater-al, normal limb, for comparison purposes). In many instancesthis is a reasonable approach (e.g., a young, otherwise healthyman with major nerve injuries in one upper limb). However,in other instances it is a major obstacle to diagnosis (e.g.,

10 Evaluating and Treating the Injured Worker AANEM Course

patients with brachial plexopathies or elderly diabeticpatients with unilateral distal lower limb injuries). In somesituations, it is impossible to determine the significance of aparticular EDX finding obtained on the symptomatic limbwithout having results obtained on the contralateral normallimb to which to compare it. Administrative factors may alsobe limited to the work site. The injured worker may beunable to obtain any workplace accommodations, such asmodified or light duty, because the employer is unwilling orunable to provide these accomodations.8,19

Obviously injured workers may have a number of reasons forresisting a return to work. Moreover, many of these factorsare operative at the time of the initial evaluation and theyoften seriously compromise the physical examination, partic-ularly in regard to suspected PNS injuries. Thus, the proce-dures employed during the physical examination to assess themuscle strength integrity of the PNS rely on the patient per-forming maximal effort. Similarly, when testing sensory func-tions or determining symptoms produced with provocativemaneuvers, the patient’s honesty in reporting is necessary. Insituations in which patient efforts or veracity are questioned,EDX examinations often prove helpful, since they can pro-vide objective results compared to those obtained during thephysical examination.7

Many physicians who order EDX examinations for injuredworkers do not perform the procedure themselves, and knowlittle about its characteristics, particularly in regard to its lim-itations. In this author’s experience, they often are doublyunenlightened. First, they are oblivious to the circumstancesin which the EDX examination should be obtained, becauseit will provide information useful in patient management.Second, they frequently display unrealistic expectations ofthe EDX examination’s capability to provide diagnostic helpin situations in which it is extremely unlikely to do so.

LIMITATIONS OF THE ELECTRODIAGNOSTIC EXAMINATION

The major limitations of the EDX examination should beexplained to all physicians who request such studies on theirpatients.

Virtually all components of the standard EDX examinationassess only large myelinated fibers, specifically, the motorfibers that transmit impulses to the extrafusal muscle fibersand the sensory fibers that convey impulses dealing withposition, vibration, and light touch. Pain fibers, beingunmyelinated, are not evaluated by any component of theEDX examination. Consequently, if pain is the sole symp-tom, the EDX examination is not likely to be revealing unlessthe pain is due to a PNS lesion which has concomitantlydamaged large myelinated fibers and evidence of the latter is

still detectable on either the NCSs or the needle EMG (orboth).33

The ability of the EDX examination to detect a specific PNSdisorder varies enormously, based on the particular injury inquestion and its duration. This is important point becausemany physicians are aware of the high sensitivity the EDXexamination has for identifying CTS and they erroneouslyassume that it is equally sensitive for detecting all other PNSdisorders. For example, most patients who have intermittentparesthesias in the median nerve-innervated fingers becauseof CTS have positive EDX examinations; however, manypatients who have similar sensory symptoms in the ulnarnerve-innervated fingers because of an ulnar neuropathy atthe elbow have completely normal EDX examinations.Physicians who do not know that the EDX examination’scapability to identify a lesion varies substantially may mistak-enly assume that a particular PNS disorder has been exclud-ed by a normal EDX examination when it has not. This canlead to their attributing their patients’ symptoms to someother PNS disorder or even to psychogenic factors.

The EDX examination can detect the presence of a lesionand provide useful information regarding its pathophysiolo-gy, severity, and extent, but generally cannot establish its eti-ology. It is difficult to assess patients with possible work-relat-ed injuries in this regard, because the injury’s cause is oftenquestionable. Typically, the EDX findings concerning etiolo-gy are noninformative, so the referring physician must relyheavily on the history—often provided only by the patientand which may be self-serving. However, there are a fewexceptions. The EDX findings of acute compression of themedian nerve in the carpal tunnel are distinct from those typ-ically seen with chronic compression of the same nerve at thesame location (i.e., CTS). The former findings are oftenincorrectly referred to as “acute CTS,” which is a contradic-tion in terms because CTS by definition is due to chronicnerve entrapment. Acute CTS results from abrupt injury ofthe median nerve within the carpal tunnel and its pathophys-iology is either demyelinating conduction block or conduc-tion failure caused by axon loss. In contrast, CTS is caused bychronic or subacute compression of the median nerve withinthe carpal tunnel, and its characteristic pathophysiology isdemyelinating conduction-slowing until it is far advanced.Because of these different pathophysiologies, the clinical andEDX features of these two types of median nerve lesions aredissimilar. Patients with acute CTS clinically manifestmarked weakness of the median nerve-innervated thenarmuscles and fixed sensory deficits in the median nerve distri-bution in the hand and fingers. During the EDX examina-tion, the compound muscle action potentials (CMAPs)recorded from the lateral thenar (median nerve-innervated)muscles and the sensory nerve action potentials (SNAPs)recorded from the median nerve-innervated fingers usually


are unelicitable, although occasionally they are simply low inamplitude. If they are the latter, then invariably the distal andpeak latencies for the responses are normal or only slightlyprolonged (consistent with the severe degree of demyelinat-ing conduction block or axon loss present). When perform-ing needle EMG of the lateral thenar muscles, fibrillationpotentials are seen if the lesions are of 3 or more weeks dura-tion, and either no motor unit action potentials (MUAPs)can be activated, or there is markedly reduced MUAP recruit-ment. These clinical and EDX changes are unlike those seenwith typical CTS: the most prominent symptom usually isintermittent paresthesias in the median nerve-innervated fin-gers and, on EDX examination, the median NCSs are pro-longed in latency (usually with normal amplitudes) and nee-dle EMG of the lateral thenar muscles typically is normal.31

The EDX examination has little ability to “date” (i.e., todetermine the duration of ) any PNS lesions it detects. Amajor exception is axon loss injuries that are severe enough toaffect the amplitudes of the NCSs, and the latter are per-formed during the first 10 days after lesion onset. During this“hyperacute” period, the NCS findings are predictable.Following a severe, focal axon loss lesion, the CMAP respons-es on stimulating and recording distal to the lesion site arenormal for the first 2-3 days. Then they begin to progressive-ly decrease in amplitude as more fibers are unable to conductimpulses to the recorded muscle. The CMAP amplitudesreach 15% of their pre-injury height at 5 days post-injury,and their nadir by 7 days post-injury. The SNAP amplitudesalso progressively decrease on stimulating and recording dis-tal to an axon loss lesion (at least one at or distal to the dor-sal root ganglion), but they follow a different time coursethan the CMAPs. The SNAPs are unaltered for the first 5days after lesion-onset, and then drop progressively over thenext 4-5 days, reaching their nadir at day 10-11 after onset.While the motor and sensory NCS responses are decreasingin amplitude, but before they become unelicitable, the ratesof conduction along the surviving fibers remain within ornear the normal range. In any case, the NCSs with axon losslesions are as severely affected as they will be by 10-11 daysafter lesion onset. With substantial axon loss lesions, the nee-dle EMG will show reduced MUAP recruitment immediate-ly after lesion onset and will persist, whereas fibrillationpotentials develop anywhere between 10-35 days after onset,depending upon such factors as the distance between thelesion site and the muscle being sampled. To complicate mat-ters, some patients are “late fibbers” and do not develop fib-rillation potentials until several weeks (4-6) after lesion onset.With abrupt onset focal NCS lesions, detecting a demyeli-nating conduction block usually indicates the lesion is of lessthan 6 weeks duration, because most neurapractic injuries ofsuch nature resolve within that time period. On needleEMG, fibrillation potentials tend to disappear from dener-vated muscles as time passes, either because of progressive

reinnervation or because of muscle degeneration. However,the time course is variable, depending on such factors as thedensity of the fibrillation potentials initially present, and thedistance between the injury site along the PNS fibers and themuscle being sampled. In general, relatively few fibrillationpotentials are detectable in muscles which have been dener-vated more than 2 years. Complex repetitive discharges(CRDs) can help establish the duration of the lesion. Eventhough they are nonspecific (i.e., seen in both neuropathicand myopathic disorders), they generally do not appear withthe former until the lesions are of at least 6 months duration.Whenever motor axon loss has been substantial enough toresult in an appreciable amount of collateral nerve fibersprouting, chronic neurogenic MUAPs are seen. These canhelp in “dating” a PNS lesion, since they generally require atleast 4-6 months to develop. However, once present, they canpersist indefinitely.31,33

After EDX abnormalities resulting from a focal PNS lesionappear, they can be quite variable in their duration. In somestatic focal disorders (e.g., CTS), they can remain relativelyunchanged indefinitely. Conversely, with other disorders(e.g., radiculopathies) they have a notorious tendency to nor-malize with time. How stable the EDX findings are dependsprincipally on the pathology at the lesion site. The changesseen with demyelinating conduction slowing lesions often arefar more persistent than those seen with axon loss, whichbegin to resolve (or attempt to do so) almost as soon as theyappear. For this reason, there is a window of time duringwhich an EDX examination is likely to reveal abnormalitiesfollowing an axon loss lesion. The EDX examination, specif-ically the needle EMG, should be performed no sooner than3 weeks after lesion onset (to allow fibrillation potentials todevelop), but ideally within the first 6 weeks (i.e., before fib-rillation potentials may begin to disappear from musclesbecause of collateral sprouting).33

Generally, EDX examinations are not as helpful as detailedhistories and clinical examinations in situations with multi-ple confounding factors. Thus, if the findings on the clinicalexamination are so complex and confusing that they areunintelligible, then the results of the EDX examinations arelikely to be as equally complex and confusing.

Electrodiagnostic examinations are essentially worthless inchronic pain syndromes. This is partly because pain fibers arenot assessed by the EDX examination, and partly becausemany of the responsible lesions are affecting sensory fibersproximal to the dorsal root ganglia. Also, many pain syn-dromes are due to factors other than PNS disorders.Regardless, in these patients the EDX studies are almostalways normal, or show only “anticipated” abnormalities(e.g., absent H response or chronic neurogenic MUAPs in adistal S1 distribution in a patient who underwent prior lumbar


laminectomy for an S1 radiculopathy). A critical point is thatthese findings in this situation have no exclusionary value—specifically, they do not exclude ongoing compression of pre-ganglionic sensory root fibers.31,32

The workplace is diverse, which means the type and severityof injuries that employees can sustain are variable. Even whenrestricted to PNS and various musculoskeletal injuries, thediversity is striking. For example, almost every peripheralnerve can be injured at virtually any point along their course.In many instances, these lesions are straightforward and theirEDX presentations are identical to those seen in lesions of asimilar type that are not work-related.

Two PNS disorders responsible for a disproportionate num-ber of work-related referrals to the EDX laboratory merit spe-cial comment: lumbosacral radiculopathies and CTS.

Low back pain, with or without lower limb radiation, isprobably the most common cause for workers being referredto physicians for evaluation and treatment. Most low backinjuries occur in workers who are 20-40 years of age (similarto the age range for persons whose back injuries are not work-related). The occupations with the highest incidence of backinjuries that result in workman’s compensation are nurses,truck drivers, and machine operators.19

Most patients with low back pain do not have lumbosacralradiculopathies and, hence, if EDX examinations are per-formed they will be normal. There are certain facts regardingthe EDX assessment of lumbosacral radiculopathies, includ-ing those that are work-related, that must be appreciated.First, the timing of an EDX examination is critical if it is toreveal evidence of a radiculopathy. The study must be per-formed during the period when any fibrillation potentialspresent have had time to develop fully, but not yet had timeto disappear because the muscle fibers generating them havebeen reinnervated via collateral sprouting. Too often in thisauthor’s experience, for one reason or another, worker’s com-pensation cases referred for EDX examination have had stat-ic symptoms for many months to years. Such late referralsalmost guarantee that, even if a radiculopathy were present, itwould be undetectable on EDX examination. Second, a nor-mal EDX examination never excludes a radiculopathy, partic-ularly a chronic, static radiculopathy, because false-negativestudies are inherent to the procedure. Any physician who usessuch negative results under these circumstances to reassurethe patient that he/she does not have a radiculopathy is pro-viding misleading information.30,32 Third, EDX examina-tions and magnetic resonance imaging (MRI) studies arecompetitive procedures, not complementary, as is oftenassumed.17 Thus, usually they are helpful or unhelpful in thesame groups of patients. Because of this, if one study has notprovided useful information in a given patient, typically it is

pointless to perform the other. The majority of clinicians—with the exception of some EDX physicians—obtain MRIstudies on their patients with suspected radiculopathies,including the possible work-related ones, in lieu of EDXexaminations. Consequently, EDX examinations are not per-formed because they usually are not indicated. There are afew seldom encountered exceptions in which the EDX exam-inations can be of benefit when MRI studies cannot. The firstis when marked weakness is present with a recent onset rootlesion. If the paretic/paralyzed muscle is one that can be usedas a recording site during motor NCSs (e.g., tibialis anteriorwith peroneal motor NCSs), and the symptoms are of at least6 days duration, then the pathophysiology of the lesionresponsible for the weakness can be determined—demyeli-nating conduction block or axon loss/conduction failure.31

Also, radiculopathies caused by something other than com-pression (e.g., diabetes, mellitus, HIV, and Lyme disease) canbe detected, and proximal PNS disorders other than rootlesions (e.g., plexopathies) can be identified. A special situa-tion occurs when pregnant employees develop possible work-related radiculopathies. In these situations, the EDX exami-nation often becomes the diagnostic procedure of choice.20

Carpal tunnel syndrome is the most common human entrap-ment neuropathy. When it is suspected of being a manifesta-tion of a work-related injury, it also becomes the most con-tentious of any focal nerve lesion.5,6,18,21 More publicationshave focused on occupational CTS than any other singlework-related topic (a recent Medline search yielded over 100articles which have appeared in less than a decade).Unfortunately, the number of articles is matched only by thenumber of controversies they have generated. The followingstatement understates the major controversy: “Some debateexists within the medical, political, and business arenasregarding the strength of the associations between repetitivework-related activities and musculoskeletal disorders (includ-ing CTS).”7 This altercation is aptly illustrated by excerptsfrom two publications that appeared in 2002 which areimpossible to reconcile. The first is “at least one-half of allcases of carpal tunnel syndrome in North America appearattributable to occupational hand activities.”21 The secondstates “except in the case of work that involves cold tempera-tures (possibly in conjunction with load andrepetition)…work is less likely than demographic and dis-ease-related variables to cause CTS.”6 Virtually every aspectof work-related CTS is in dispute, including how to diagnoseit (and the value of NCSs) and, if it is found in an employee,what its relationship is to the work he/she performs.Although NCSs of various types are considered by many tobe as close to the gold standard as can be achieved at presentfor diagnosing CTS,10 they are a major part of the controver-sy. Establishing “normal” and “abnormal” has proven con-tentious.5,21 The high sensitivity reported for median NCSsin relationship to CTS, encountered in the clinical setting


with symptomatic patients, is not found in cross-sectionalworkplace screening. Moreover, the specificity is lower than itwas earlier thought to be.29

A recent report by Cosgrove and colleagues illustrates theproblem well.5 They selected 900 railroad workers from morethan 2500 who reputedly had work-related CTS. All had ini-tiated, or were in the process of initiating, legal proceedingsagainst their employer. Of the 900, 248 had already under-gone CTS surgery. Although all of the claimants reportedlyhad some type of NCS positive for CTS, the authors found(at least for the operated cases) that the EDX data …“weredifficult to interpret for reasons such as the absence of ulnaror radial distal latencies, failure to account for skin tempera-ture, poor description of techniques, or no numerical datasupplied.” All participants “were subject to a comprehensivehistory, physical examination, medical record review,” and anEDX assessment. The EDX study consisted of a “medianminus ulnar distal latency differential,” always utilizing bothmotor and sensory responses, and selectively using mid-pal-mar responses. They found a statistically significant relation-ship between CTS and body mass index, age, and wristindex. Almost all the participants were men, and most wereoverweight and relatively old. They found no association,however, between CTS and job classification. Using theirdiagnostic criteria, more than half the studied population didnot have CTS, and among the surgical cases, based on peri-operative data, they could not determine the justification foroperation in one-third of them because the NCS resultsappeared normal both pre- and post-surgery.5

Of all the work-related PNS disorders assessed in the EDXlaboratory, CTS is the only one often screened for (in most-ly asymptomatic persons), either during the pre-employmentassessment, or in the post-offer preplacement (POPP) peri-od.9 Whether such screening is beneficial also is debated.9,27

A review of the literature reveals that there is some (but defi-nitely not universal) consensus regarding patient occupationand CTS:

1) The prevalence of CTS among any patient groupdecreases significantly if the diagnosis rests on thepresence of both clinical and EDX findings, ratherthan solely on the former.2,10,12,21,24 Thus, in onestudy of dental hygienists, 42% could be classified ashaving CTS based on symptoms alone, but this fig-ure dropped to 8.4% when abnormal median NCSswere added to the diagnostic requirements.2

2) Workers in certain occupations have a substantiallyhigher risk than normal for developing CTS.Examples include those workers in the meat, fish,

and poultry processing industry, as well as those whouse vibrating tools.13,21 Conversely, workers in cer-tain other occupations, despite the fact that theyhave substantial upper limb symptoms, either haveno appreciable increased risk of having CTS (com-puter and keyboard users),1,21 or only a moderatelyincreased risk (dental professionals).8,20,28 One prob-lem in determining the prevalence of CTS in variousoccupational groups is that often little attempt ismade to distinguish one neuromuscular disorderfrom another. Thus, neuromuscular limb complaintsare common among dental hygienists, but these aremore often related to epicondylitis, particularly lat-eral epicondylitis, than to CTS.20,28

3) Abnormal median NCSs found in asymptomaticworkers probably have little predictive value inregard to whether those workers will subsequentlydevelop CTS.12,21

In contrast to the above, there is no consensus, in regard toworkers with CTS, concerning the relative contribution ofsuch factors as obesity, cigarette smoking, age, gender, andwrist index, compared to their work activities, in the genesisof their PNS disorder.5,6,18,21

CONCLUSION

The EDX examination can be beneficial in assessing workerswith reputed or definite job-related PNS injuries. However,it has many limitations which the referring physician must becognizant.

REFERENCES

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