LymeNet Law Pages
Web Resources



Title: Summary of the Opinions & Background of Dr. Leonard Sigal
Entered By: Ira M Maurer/LymeNetDate Created: 10/23/97

Internet URL:


Completed residency in 1979.

Board certified in Rheumatology.

Not trained in infectious diseases.

Joined Robert Wood Johnson faculty in 1988

Sees patients on Tuesday in pm and Friday in am

Enrolled 1391 people in Lyme Disease Vaccine Efficacy Trial in 1993.

Sigal doesn't consider himself to be "a leading authority" in the Lyme Disease field

LITIGATION RELATED WORK

Divorce case in Westchester County, NY where he was the expert for the father. Mother was a doctor who prescribed anti-biotics for her child. Sigal found no evidence child had Lyme Disease.

Divorce case in New Jersey where wife claimed she had Lyme Disease and couldn't work. Sigal was the husband's expert and found little basis for wife's Dx. with L.D.

Plaintiff's expert against Dr. Shah. Sigal found No L.D.

In each of these cases, Sigal has always testified that Lyme Disease is not the
correct Diagnosis or that Lyme has been overdiagnosed .

Sigal gets $450 per hour for his fee in these matters.

Sigal reviews approx. 1 case per month for attorneys, mostly on Lyme.

INSURANCE COMPANY WORK

Sigal has done work for insurance companies for last 4 years .

Sigal doesn't work for a specific company).

Sigal charges $450 pr. hr.

Most of these matters deal with Lyme Disease.

Sigal has reviewed a few dozen files for insurance companies since 1992...maybe
between 25-50.

Sigal's work for insurance companies pertains to insurance coverage for treatment
or continued treatment of Lyme Disease.

Sigal has only reviewed "a few" insurance cases where he thought the patient had
Lyme disease.

Some insurance companies have begun limiting coverage for prolonged intravenous antibiotic therapy. Patients view this as an abrupt and unjustified abrogation of their right to receive any and all treatments recommended by their"experts" for LD, which they believe to be a severe, chronic debilitating disease. The alternative interpretation is that limiting prolonged therapies is an attempt to limit unnecessary side effects and toxic effects of the therapy in patients with documented LD and those who do not have LD. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1498


TICK INFORMATION

80% of all Lyme Disease cases start in June and July. Conn's Current Therapy,
1993; Lyme Disease Method of Leonard H. Sigal at p 124

It is important to know what the risk of getting LD is from a known tick bite. 10% -20% of nymphal Ixodes Dammini carry B. Burgdorferi. Rheumatic Disease Clinics of North America; Vol 19. Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p86

The real degree of risk of acquisition of Lyme disease is very small and does not justify prophylactic therapy for an "otherwise asymptomatic tick bit with no clinical sequelae" Drugs 43, 1992; Current Recommendations for the Treatment of Lyme Disease at p692

Our suggestion is that if no skin rash develops and no signs or symptoms suggestive or Lyme disease develop, the bitten individual should return for blood testing at 6-8 weeks after the bite; if seropositive, the patient then can be treated with an oral regimen. New Jersey Medicine, Vol 87, Number 6, July 1990, Clinical Manifestations of Lyme Disease; page 554

LYME DISEASE DIAGNOSIS

Lyme Disease is a clinical, not a serologic or laboratory, diagnosis. Rheumatic Disease Clinics of North America, Vol 19, Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p 79.

Lyme Disease is a multisystem inflammatory disease caused by infection with Borrelia Burgdorferi. Drugs 43, 1992; Current Recommendations for the Treatment of Lyme Disease at p. 684

Several factors contribute to overdiagnosis of Lyme Disease. Some physicians may have been encouraged to rush to this diagnosis by opportunities for financial gain-for example, some received payments from infusion companies involved in long-term intravenous therapy. Hospital practice, May 15, 1996; Editorial .

Marked variation is possible in the clinical expression of the disease. Clinical Manifestations of Lyme Disease, 1986 Steere, Bartenhagen, Craft, Hutchinson, Newman, Pachner, Rahn, Sigal, Taylor and Malawista at p 204

Early Localized Disease is characterized by Erythema Migrans in 50-70% of patients; Nonspecific symptoms ("viruslike syndrome") include fatigue, malaise, lethargy, headache, myalgia, arthralgias and regional or generalized Lymphadenopathy. These occur a few days to a month after the tick bite. Hospital practice, May 15, 1996; Editorial.

Soon after the tick bite which transmits the infection, the ECM rash occurs in 50-70% of patients, often with associated symptoms resembling a "summer cold" or viral infection. Drugs 43, 1992; Current Recommendations for the Treatment of Lyme Disease at p 684.

Probably due to spirochetemia (dissemination of the organism), secondary lesions occur and may be oval or round nondescript erythematous macules or papules. Conn's Current Therapy, 1993; Lyme Disease Method of Leonard H. Sigal at p125

There is a correlation between severity of the intial illness or the presence of multiple ECM lesions with progression to later LD Conn's Current Therapy, 1993; Lyme Disease Method of Leonard H. Sigal at p 125

Early Disseminated Disease includes: Heart problems-Carditis (8-10% of untreated patients), Conduction defects, Mild cardiomyopathy, Myopericarditis. These occur days to 10 months after the tick bite. Hospital practice, May 15, 1996; Editorial.

The clinical findings of carditis include fluctuating atrioventricular conduction defect (first, second, and complete heart block), tachyarrhythmias, and myopericarditis, very mild congestive heart failure, bundle branch block block. Conn's Current Therapy, 1993; Lyme Disease Method of Leonard H. Sigal at p126 Early disseminated disease also manifests itself with neurologic (lymphocytic meningitis, peripheral and cranial nerve palsies, encephalitis), or both. Some patients with early disseminated LD do not recall EM or a prior illness suggesting LD. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p.1494

Progression to musculoskeletal features of LD is common in untreated LD; 80% of
patients may experience noninflammatory or inflammatory joint disease in months to years. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at
p1494

Late Lyme Disease (Tertiary Neuroborreliosis)- features different neuroloci complication, including peripheral neuropathy, encephalopathy, and neuropathy,
encephalopathy, and neuropsychological problems. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1494

Late LD may be the initial feature of LD. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1494

Lyme Disease may have rapidly progressed to what are considered later
manifestations. The American Journal of Medicine, Vol.98 4/24/95 (suppl 4A), Anxiety and Persistence of Lyme Disease at p4A-76S

The Jarisch-Herxheimer reaction, occurs in 15% of patients within 24-48 hours of the start of therapy. The American Journal of Medicine, Vol 96, April 1994; Persisting Complaints Attributed to Chronic Lyme Disease: Possible Mechanisms and Implications for Management at p.372

FIBROMYALGIA

Fibromyalgia Syndrome (FMS) is common in general medical and rheumatology
practices. Its pathogenesis is probably related to muscle deconditioning and sleep
disturbance; it is known that persistent disruption or reduction of stage 4 sleep is common. There may be chronic generalized immune activation with elaboration of several cytokines; cytokine infusion can cause sleep disorder. Prolonged inactivity from pain and fatigue may result and cause further muscle deconditioning. Arthritis & Rheumatism, Vol 36, Number 11, Nov. 1993; Chronic Lyme Disease as the Incorrect Diagnosis in Patients with Fibromyalgia at pp 1498-1499.

The majority of the patients with fibromyalgia seen in the New Jersey clinic had prior or active Lyme disease. . Arthritis & Rheumatism, Vol 36, Number 11, Nov. 1993 ;Do Infections Trigger Fibromyalgia? at p 1490. Fibromyalgia's fatigue, cognitive dysfunction, and musculoskeletal pain can be misinterpreted as central nervous system Lyme disease or Lyme arthritis. Hospital practice, May 15, 1996; Editorial.

Fibromyalgia is treated with tricyclic antidepressants in non-therapeutic doses at
bedtime and with exercise.

Lyme is often an incorrect diagnosis in pediatric and adolescent fibromyalgia (Sigal paper in Pediatrics, Oct. 1992).

We see alot of people with a history that is at least compatible with Lyme disease who meed the criteria for fibromyalgia: They are seropositive, we have reason to believe they have been exposed to Borrelia Burgdorferi, and they have been treated. The question is, do they have central nevous system Lyme disease with a subtle encephalopathy,or, in fact, do they have fibromyalgia. The American Journal of Medicine 4/24/95 Vol 98. A Symposium: National Clinical Conference on Lyme Disease; Neuroborreliosis discussion.

Many nonrheumatologists have not hear of fibromyalgia or do not believe that it is a distinct clinical entity. As Johann Wolfgang von Goethe said, "was Man weiss Man sieht" (What one knows, one sees). Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1495

SEROLOGIC TESTS

The serologic tests now available...ELISA (enzyme-linked immunosorbent assay) and Western Blot to confirm equivocal or positive ELISAs are quite good in confirming the diagnosis of Lyme Disease.(The American Journal of Medicine, 4/24/95 Vol. 98 Epilogue).

Some patients with ongoing infection may serorevert after therapy. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p.222.

If persistent symptoms are accompanied by significantly rising levels of antibody or the appearance of reactivity with new bands on immunoblot, ongoing infection must be considered. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p. 222.

The incidence of false-positive ELISA results in normal persons is about 4% nationwide. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at 1495

The suggestive terms "LD serologic test" and "LD ELISA" should be abandoned in
favor of the less suggestive and more accurate term "anti-B Burgdorferi seroreactivity". Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1496

Seroconversion may take up to 6 to 8 weeks followin a tick bite, not because the test is flawed but because there are no free serum antibodies to be detected. Thus patients with early LD may be sero-negative. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1496

LD serologic tests are usually negative in the first 2-3 weeks of illness and
seroconversion may develop as long as 6-8 weeks into the disease. Conn's Current
Therapy, 1993; Lyme Disease Method of Leonard H. Sigal at p 125

Sigal is concerned "about the person who comes with a positive serologic test -usually an ELISA-as proof of LD, but who also has had 17 negatives. If you test often enough you will generate a positive ELISA. So the kind of person you are describing never shows up in my office without having been repeatedly tested and usually abused with at least two courses of antibiotics. The American Journal of Medicine, Vol.98 4/24/95 (suppl 4A), Anxiety and Persistence of Lyme Disease at p4A-79S

Western Blotting has 3 limitations to the technique:(1) even Western blotting may be negative in very early disease; it may take up to 6 weeks for a patient to produce sufficient antibody to be detected; (2) after antibiotic therapy, even unsuccessful therapy, there may be loss of reactivity, even in Western Blotting; and (3) some laboratories provide inaccurate interpretations with their reports. Rheumatic Disease Clinics of North America; Vol 19. Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p84.

Early, even inadequate, antibiotic therapy can blunt or totally abrogate the
immunoglobulin response in LD representing a potential cause for false seronegativity in later disease as well. Rheumatic Disease Clinics of North America; Vol 19. Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p85

One study suggest that follow-up testing in LD is usually not helpful. A decrease in serum antibody levels does not prove resolution of LD, and persistence of elevated levels does not mean that the infection has not been cured. Rheumatic Disease Clinics of North America; Vol 19. Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p85

There is no correlation whatsoever between antibody levels and the ultimate outcome of a patient. Like wise, very high antibody levels can be seen in very mild disease and very low levels can be seen in patients with very severe disease. Thus, no prognostic value can be read from the level or titer of antibody in a given patient. Rheumatic Disease Clinics of North America; Vol 19. Number 1, Feb 1993; Lyme Disease: Testing and Treatment at p86

SERONEGATIVITY

Although patients with later features of Lyme Disease are usually seropositive, it is
possible for a patient to have early disseminated Lyme disease (eg. carditis, meningitis, peripheral neuropathy, or facial palsy) and be seronegative. JAMA, Nov.1995 Vol 274, No. 18 letter to the Editor on Diagnosis of Lyme Disease.

In patients with the earliest features of Lyme disease, the diagnosis may be made despite seronegativity. JAMA, Nov.1995 Vol 274, No. 18 letter to the Editor on Diagnosis of Lyme Disease.

Persistence of B. Burgdorferi seroreactivity long after LD treatment and cure has led to excesses in therapy and attendant drug and intravenous line related morbidity, based on the mistaken assumption that persisting seropositivity equates with persisting infection. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

POSSIBLE EXPLANATIONS FOR PERSISTENCE OF
SYMPTOMS AFTER ANTIBIOTIC THERAPY FOR
LYME DISEASE

Slowly Resolving Lyme Disease- As many as 50% of patients develop nonspecific complaints (headache, fatigue, lethargy, and noninflammatory musculoskeletal pain) after therapy for early or late Lyme Disease. These complaints are usually self-limited and do not respond to further antibiotics. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

Lyme arthritis rarely improves immediately; inflammation may persist for as long as 8 months after completion of therapy. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

The finding of chronic neurologic Lyme disease may resolve gradually; sensory and motor symptoms may persist for more than 6 months, peripheral neuropathy and radiculitis taking 24 months or more to abate, perhaps because nerve regeneration is relatively slow. Tertiary neuroborreliosis may take many months to resolve, and residual deficits have been documented. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

Permanent Tissue Damage - Irreversible changes in tissues caused by previous infection do not improve with further antibiotic therapy. If therapy for LD is delayed, it is possible that tissue damage caused by the infection may be irreparable, resulting in permanent organ dysfunction. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

Damage persisting after antibiotic therapy has been described in LD patients with facial nerve palsy, central or peripheral nervous system disease, heart block, and arthritis. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

The likelihood of permanence correlates with duration of disease prior to initiation of therapy and severity of the initial features of LD. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

In cases in which tissue damage is irreversible, it is wise to shift the emphasis to
rehabilitation rather than to more ineffective antibiotics. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.

Factors Related to Chronic Illness-Fibromyalgia may occur after LD as part of a post-LD syndrome. Treatment of fibromyalgia with antibiotics did not improve our patients' fibromyalgia. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy. p.223.

Truly Persisting Infection with B. Burgdorferi-Patients with proven persistent B. Burgdorferi infection may benefit from further antibiotic therapy and should be re-treated. In the initial controlled studies of antibiotic therapy for LD (using lower dose and shorter duration of therapy than are now suggested), some patients improved during treatment only to relapse later. Many such patients can be cured by treatment with a longer duration or highter dose of antibiotics or by a change to use of an alternate agent; intravenous therapy may be needed, depending on the feature of LD present. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p.223.

The likely explanation for lack of response to therapy is that the original regimen was inadequate, either in duration or in method of delivery, or that the patient was noncompliant with the orinial regimen. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p223

In some patients there may be progression to later features of LD despite appropriate prior treatment. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p223

One possible explanation is the proven early dissemination of the organism to the
central nervous system and elsewhere. The regimens appropriate for isolated erythema migrans may not eradicate the organism from such a hidden focus. If the patient has erythema migrans and asymptomatic dissemination, the clinically indicated oral therapy may not be adequate to treat the other, unsuspected foci of infection, because of insufficient tissue penetration of drug. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p223

It is difficult to explain relapses occuring within hours to days of termination of therapy (common in our endemic area) on the basis of regrowth of the organism, given the relatively long (ll to 12 hours generation time of the organism. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p224

Some patients have objective evidence of relapse despite treatment with what is generally considered to be an appropriate regimen for the clinical features of that patient. In such a circumstance, re-treatment with detailed clinical follow-up is indicated. We recommend a different drug or longer duration and/or higher dose of the previous agent for the second course of treatment. Lack of response to the first treatment may represent true treatment failure: there may have been inadequate absorption or penetration of the first drug to privileged sites in which the orgnism resided; resistance; resistance; intracellular survival of the organism. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p224

Sterile Inflammation caused by Dead Organism-Dead or live organisms can cause immune cells to produce a variety of cytokines in vitro. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p224

Persistence of arthritis after therapy can occur and may be due to mechanism other than infection, which may include local antigen-specific reactivity directed at poorly degraded persisting antigens, local nonspecific inflammatory or immunomodulatory effects due to local production of cytokines, and vasculopathy or vasculitis due to inflammation in or near vessels. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p224

Possible Immune Phenomena After Lyme Disease-Most, if not all, of the clinical features of early LD are related to local infection. Antigen-specific immune reactivity, both humoral and cellular, is increased locally and systemically. Nonspecific immunologic changes also have been noted. If the late features of LD were due solely to ongoing infection, antibiotics would be expected to be universally effective. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p224

The immunologic phenomena seen in LD may be involved in the pathogenesis of LD, especially in the proposed link between B. Burgdorferi infection and postinfectious reactive arthritis. In one study, the absence of response of joint inflammattion to antibiotic therapy in eight of nine patients led the authors to suggest that the synovitis was due to a reactive phenomenon rather than to ongoing infection. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p225

Autoimmunity may be a cause of LD related neurologic damage, based on immunologic cross-reactivity between a component of B. Burgdorferi and a human axonal protein. The phenomen is called molecular mimicry: a component of an infectious agent resembles a component of host tissue, and the immune responce to the organism then elicits reactivity that can attack and damage the host. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p225

In summary, if the initial diagnosis of LD was correct, possible explanations for persistence of symptoms include inadequacy of prior therapy, slow resolution of LD after (ultimately) successful therapy, persistence of poorly degraded antigen on nonviable organisms, permanent tissue damage from prior infection, and evolution of immune processes not requiring the presence of viable organisms. Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p226

Persistence of Infection could be due to the organism taking refuge within cells or
in isolated foci, eg. the central nervous system. The Journal of Rheumatology
1994; 21:4 Persisting Symptoms of Lyme Disease-Possible Explanations and
Implications for Treatment at p 594

NO TEST AVAILABLE CAN DIFFERENTIATE
BETWEEN BACTERIOLOGIC CURE WITH
PERSISTING SYMPTOMS AND PERSISTENT ACTIVE
INFECTION. Rheumatic disease Clinics of North America; Vol. 21, Number
1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p226



EXTENDED TREATMENT OF LYME DISEASE

In the presence of active infection after antibiotic therapy, it is important to consider the prior treatment: dosage, duration, type of delivery, and compliance. If there is reason to believe that prior oral therapy has been insufficient or unsuccessful, intravenous antibiotics are suggested. . Rheumatic disease Clinics of North America; Vol. 21, Number 1, Feb. 1995; Management of Lyme Disease Refractory to Antibiotic Therapy.p.222.

A small proportion of patients receiving a ppropriate therapy do not respond. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1494.


LYME DISEASE COUNTER-CULTURE

A Lyme Disease counter-culture has emerged that takes the honest caveats and
manipulates them to give the public a set of certainties: Don't trust tests, they are worthless; don't trust standard thrapies, they are ineffective; don't accept "their" arguments that your infection is really cured, they are lying; don't trust the
medicalestablishment, the academis are conspiring against us. Archives of Internal
Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1497.

The diagnosis of chronic, resistant LD is encouraged "by some infusion companies and their associated local experts and then supported by patient advocacy and support groups and their associated local experts; some infusion companies pay such practitioners for referrals, raising the question of conflict of interest. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1497

In some areas of the country, there is widespread fear that LD will not respond to
anti-biotic therapy and will inexorably progress to later manifestations of the infection. This has led to more anxiety about the disease and has added a sense of urgency to the desire to make the diagnosis as early as possible. Increasingly, patients living in areas endemic for LD who have arthralgias, myalgias, chronic fatigue, difficulties with concentration or memnory, mild paresthesias or headaches, with or without a prior history of LD are diagnosed as having "chronic", "persistent", "resistant", or previously "dormant" LD. Pediatrics, vol. 90, Oct. 1992; Lyme Arthritis as the Incorrect Diagnosis in Pediatric and Adolescent Fibromyalgia at p 523

Some local clinicians have established practices limited to LD, ensconcing themselves as "LD experts." Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1498

Patients and families are aware of the possible late manifestations of Lyme disease and are increasingly anxious about possible long-term and irreversible damage that might result if the diagnosis of Lyme disease is missed. The American Journal of Medicine, Vol 88, June 1990, Summary of the First 100 Patients Seen at a Lyme Disease Referral Center at p 580

Even more anxiety is produced when a Lyme disease counterculture is willing to
diagnose Lyme Disease when others will not. A seed of doubt concerning the family doctor and the medical establishment is planted and takes root. The American Journal of Medicine, Vol.98 4/24/95 (suppl 4A), Anxiety and Persistence of Lyme Disease at p4A-77S

CDC CRITERIA

The Center for Disease Control criteria are not a set of diagnostic criteria: rather, they are an epidemiological definition of an incontrovertible case of LD. Anger about the CDC criteria is unfounded and represents a misunderstanding of the purpose of the criteria, which is to allow year-to-year variation in the number of reported cases in an area to be charted and new foci of disease to be identified. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1497

UNDERDIAGNOSIS AND UNDERTREATMENT OF LD

Some clinicians still do not recognize LD, do not include LD in the appropriate
differential diagnoses, and do not use appropriate treatment regimens. Failing to diagnose and treat LD early in its course can lead to increased severity of disease
and to progression of disease, eg. LD that is unrecognized while the patient has EM may progress to neurologic or articular disease with added morbidity and expense in diagnosis and treatment. Archives of Internal Medicine, Vol 156, July 1996, The Lyme Disease Controversy, Social and Financial Costs of Misdiagnosis and Mismanagement at p1497

Missing the diagnosis early may cause long-term, occasionally permanent, disability. Thus, timely diagnosis and treatment are important. The Journal of Infectious Diseases; 171:423-4; Editorial: Lyme Disease: Primum Non Nocere at p 423



The Lyme Disease Network of NJ, Inc.
43 Winton Road
East Brunswick, NJ 08816
http://www.lymenet.org/