Continued from Part 1...
Dr. John Bleiweiss
When To Suspect Lyme
LD could cause reversible disturbances in brain physiology through cytokine mediators, direct infection; e.g., encephalitis and perivasculitis, demyelination, metabolic aberrations within the CNS such as regional hypoperfusion, altered rheologic (flow) characteristics of blood, intracellular acidosis and the depletion of ATP. Permanent changes may include demyelination or loss of neurons leading to atrophy.
Neurologic complications in earlier reports were said to occur in 20% of LD cases. In my experience, and as published by Dr. Logigian, 90% of patients have one or more of encephalopathy, cranial neuritis or psychiatric changes. Early in the course of LD, these problems may be absent or muted, but eventually intrude and can become dominant aspects of LD.
Many patients are told that they have Multiple Sclerosis (MS) because of brain MRI findings or a spinal tap was positive for oligoclonal bands (OCB) or myelin basic protein (MBP). The medical literature is quite emphatic that MRI does not reliably distinguish between MS an LD because there is too much overlap in their supposedly distinct appearance and location of plaques. Plaques have been detected with both disorders in the brain and spinal cord. OCB's and MBP are non-specific markers for demyelination (loss of sheath around nerves) and do not signify a cause of the demyelination. In Miklossy's study above, senile plaques stained avidly for Bb spirochetes. Vincent Marshall reviewed the MD literature in Medical Hypothesis (Vol 25: 89-92, 1988) and advances the notion that LD is causing MS! His survey revealed that multiple studies prior to 1951 were able to demonstrate spirochetes in the spinal fluid of MS patients (by inoculation into animals and on silver stain of CNS tissues). Dr. Coyle has documented the presence of antibodies to Bb in MS patients (Neurology Vol. 39:760-763, 1989). The encephalopathy attributed to MS is very reminiscent of LD. Both MS and LD are associated with sinusitis (Lancet, 1986). Dr. Leigner has reported a case of LD which fulfilled all criteria for MS. The epidemiology of MS and the geographic distribution parallels that of LD. The symptoms of both LD and MS can be aggravated if the patient takes a hot bath. Anecdotally, patients with LD, who previously had been identified as MS, responded to antibiotic therapy.
LD has been documented to cause strokes, paralysis, a variety of seizures, transient or permanent blindness, Parkinsonian-like movement disorders, motor and/or sensory neuropathies, mononeuritis multiplex, radiculoneuritic pains, meningitis and encephalitis. It has been affiliated with Lou Gehrig's disease and the Guillain-Barre Syndrome.
Recent reports suggest that the spectrum of neurologic LD is actually similar in both Europe and the USA (Jacqueline, MS; Surv Opthalmol 35:191-204, 1990) and belies the assertion that European LD research holds no relevance for LD in the USA.
The more commonly noticed neurologic deficits involve one or more cranial nerves (I thru XII), most often the sensory divisions of the trigeminal (V) and the motor components of the facial (VII) nerves in my patients. In declining order, deficits to pain sense are detected in V2, V3, and V1. V2 neuritis appears as paraesthesias or dullness in the central face and cheeks. Gum and tooth pain can be another manifestation of trigeminal neuritis. Rule out dental abscess or sinusitis which can present with similar tooth pain.
The most common cranial neuritis I see is that of the VII nerve. Abnormalities of the VII nerve can be varied. Usually there is symmetry of the central facial creases, the lips at rest or in motion, or overt deviation of the mouth or smile to one side. Colleagues have dismissed these asymmetries as normal findings, saying "well, everyone has those". I feel there is significance when antibiotics cause these so-called innate or normal findings to resolve.
When Bell's palsy is present, there are the facial defects described above for VII neuritis plus a wider eye on the same side as an elevated eyebrow, often attended by complaints of tearing and drooling (usually at night) on the affected side. 10.6% of 951 LD cases were found with Bell's palsy and 25% of those have had bilateral Bell's palsy (Clark, JR et al. Laryngoscope 1985: 95: 1341-45). Bilateral Bell's promulgated as pathognomonic for LD, actually can be associated with intrapontine lesions, diabetes mellitus, syphilis, sarcoid, leukemia, Guillain-Barre, viruses or diphtheria. Considering the incidence of Bell's palsy in LD, it is improper to treat it as viral in origin without a work-up for LD.
Incidentally, hyperaccusis (sound sensitivity) can be a feature of VII neuritis. Olfactory neuritis (I) is attended by dysosmia (unusual smells). Neuritis of the III, IV and VI cranial nerves will show up as double vision. When the VIII nerve is involved, vertigo and impaired hearing can result. I have had at least two cases of Meniere's Disease respond to treatment for LD. Dysphagia (difficulty swallowing) can be associated with X neuritis but not invariably. More often in my experience, a deviated uvula or soft palate is perceived. Dysphonia (altered voice) can occur with X neuritis when the branches that serve the larynx are affected. Recurrent laryngeal nerve paralysis has been seen with LD (Schroeter, V. et al. Lancet 2:1245, 1988). IX neuritis (glossopharyngeal) can cause a unilateral sore throat which was reported by 3 of my patients. XI neuritis (spinal accessory) presents as trapezial or sternocleidomastoid muscle weakness resulting in a drooped shoulder or weakness on resisted head rotation respectively. Do not confuse this with a unilateral dystonia where the affected shoulder girdle will be elevated with preserved motor strength on both sides. Hypoglossal (XII) neuritis can be associated with a heaped up tongue on the unaffected side or deviation of the tongue on protrusion toward the abnormal side.
LD related headaches can have a wide variety of patterns and can broadcast the early onset of LD or a flare of LD. The headaches incorporate the characteristics of migraines, muscle tension or cervical/radicular headaches. Pseudotumor cerebri (elevated CSF pressure with normal CSF analysis in the absence of intracranial masses) can complicate the course of LD and cause headaches. Papilledema (swelling) of the optic disc is usually present when CSF pressures are elevated, but not invariable. A spinal tap will have high opening pressures and be therapeutic as well. Depending on the characteristics of the headaches, sinusitis and brain tumors may have to be ruled out. Cluster headaches have characteristics compatible with some LD headaches including responsiveness to 100% oxygen.
Immunosuppression due to LD has been reported. Therefore, it is not surprising that recurrent or intractable upper respiratory tract infections (URI's) have been noted. LD can cause or worsen pre-existing sinusitis, asthma, bronchitis, otitis, mastoiditis. Frequently, the pediatric history of LD contains a pattern of repetitive URI's. Mastoiditis can also be associated with a Bell's Palsy. LD can be affiliated with the appearance of new onset allergies for the first time in a patient's life or magnify an atopic predisposition. The usual medications for sinusitis and allergies will have a predictably diminished effect, when LD is operant.
Another concomitant reported by an incidental patient is the occurrence of motion sickness which can be reversed with LD treatment.
Eye related problems in LD are commonplace and can include conjunctivitis, ocular myalgias, keratitis, episcleritis, optic neuritis, pars planitis, uveitis, iritis, transient or permanent blindness, temporal arteritis, vitritis and periorbital edema (Jacqueline MS; Ibid). Horner's syndrome, ocular myasthenia gravis, and an Argyll-Robertson pupil are also reported. Optic neuritis has been observed to become recurrent or intractable after treatment with steroids. Given the earlier remarks about the detrimental effects of steroids on LD, recidivous optic neuritis may be due to occult LD.
Lyme hepatitis occurs in approximately 15-20% of patients. Liver tenderness is inconstant and the elevated liver enzymes respond to antibiotics. Sometimes, the hepatitis appears temporarily in the early phases of treatment with subsequent resolution.
In many of my patients, cysts are found not uncommonly in various locations: thyroid, breast, liver, bone, ovary, skin, pineal gland, and kidney. Some forms of Polycystic Kidney and Fibrocystic Breast Disease may be LD manifestations.
LD can cause an interstitial cystis leading to bladder pain relieved by urination. A neurogenic bladder can develop with either hesitancy, frequency, loss of bladder awareness, urinary retention, incontinence or the symptoms of UTI (urinary tract infection). I suspect that some cases of chronic pyelonephritis are actually LD. Pediatricians may want to consider that nocturnal enuresis (bedwetting) is secondary to LD.
Constipation severe enough to cause fecal impaction can occur. Many LD patients will experience a spastic (irritable) colon and that diagnosis should spark a search for LD. I have treated LD attended by ulcerative colitis with substantial remission of the colitis when antibiotics were inaugurated. Fecal incontinence due to impaired rectal sphincter tone can occur. Dr. Martin Fried has demonstrated Bb spirochete in the gastric and duodenal mucosa of children with LD who complained of abdominal pain and who were documented to have gastritis and/or duodenitis. It is appropriate to work up LD when confronted by these clinical entities.
Among untreated patients with LD, arthritis can ultimately develop in up to 60%. The joint swelling, which may or may not be painful, frequently is episodic, recurrent and migratory if multiple joints are involved. Any joint can be affected including the TMJ (temporomandibular) and small joints of the fingers (contrary to earlier reports). Up to 10% of untreated LD arthritis can develop into destructive/deforming synovitis almost identical to Rheumatoid Arthritis (RA). Dr. Lavoie has published the coincident findings of LD with RA, and SLE (lupus) with LD. The SLE was associated with positive DS-DNA (double stranded DNA) which is considered diagnostic for lupus. This marker improved with antibiotic treatment for the LD. The author felt that the LD might be causing/aggravating the SLE.
I would like to present a case of a 38 y.o. white female who, 24 days postpartum, presented with Seropositive LD. She had a prior history of a round rash 6" diameter in 6/90, DS-DNA =320 in 12/90 and previously treated Lyme (seronegative) by various physicians (including myself) from 12/90 to 12/92 with eradication of all symptoms. The patient became pregnant 7/93 and her former Lyme symptoms were revived. She declined to take amoxil prescribed by her OB-GYN until 11/93. this was followed by 10 days of Zithromax with minimal results. The exacerbation accelerated about 2 weeks prior to her 3/28/94 visit to me. In addition to Lyme, her contemporary problems included SLE, episodic Sjogren's Syndrome (dry mouth/eyes, parotiditis), anticardiolipin antibodies without thrombotic events, polyarthritis (in ankles, knees, hips, shoulders and PIP's of the fingers), a left IX neuritis, a right Bell's Palsy, ptosis of the left upper eyelid, myositis of the rectus abdominus muscle, generalized fibrositis and periostitis, degenerative changes in several finger joints and a few costochondral joints, and fibrocystic breast disease. Encephalopathy was absent! The lab findings included: Lyme Elisa IgG = 1.4 (+), Lyme IgM = 320 (++), Lyme LgM by IFA = 640 (+++), a NEGATIVE Western Blot (only 41 KDA) and IgG by IFA for LD, positive Lyme IgG Antibody in synovial fluid (Class II exudate) obtained from the right knee = 1.94, DS-DNA = 5, 120 (less than 10 is normal), ANA = 2,560 (+++), positive Sjogren antibody (SSB = 33), positive anticardiolipin antibodies (IgG = 66, IgM = 44.9), leukopenia (wbc = 2,800), and anemia (Hgb = 11.4), 10 bands and 1736 PMN's on CBC differential, ESR = 32, slightly depressed complement levels: C3 = 55, C4 = 14. Lyme PCR (a test for the DNA of Bb) in synovial fluid was negative. Concurrent vaginal bleeding prevented us from obtaining an immediate U/A.
Other lab tests : Fe = 34, Ferritin = 64, transferrin saturation = 9.36%, Bun = 18, Creatine - 0.9, Rheumatoid Factor and SSA negative; thyroid and coagulation profiles, TSH and PTH normal; CH50 = 222, CXR and EKG noncontributory.
The patient acutely developed (after using Motrin on her own, instead of the prescribed Percocet for relief of arthralgias while the work up was in progress) leukopenia (wbc = 1,700),neutropenia (PMN's = 1,074), and an acute hepatitis with abnormal liver enzymes (LFT's) : Total Bilirubin = 1.58, alkaline phosphatase = 328, LDH = 344, GGTP = 113, SGOT = 246, SGPT = 285.
Within 72 hours of stopping Motrin use, the wbc rebounded to 4,700 but by then the patient had developed an acute partial paralysis of her legs (3/5), with deltoid, biceps and vastus lateralis myositis, a new left VII neuritis, and the polyarthritis was more ebullient and painful. A fever of 101 degrees F had appeared. Subsequently, hypertension (BP = 154/94), a small posterior pericardial effusion and hypokalemia (K+ = 3.3 mmol/L) were appreciated. Urine and Blood Cultures were negative. Urine analysis (U/A) contained 30-35 wbc, but proteinuria and cylindruria were absent. Elevated LFT's were again encountered. The patient declined, at various times: an MRI of brain, a bone marrow aspiration, spinal tap, EEG, and EMG.
On admission to the hospital, IV Claforan was initiated. At 41 hours, a crescendo J-H reaction attained a fever apex of 103 degrees F, but the wbc count again fell to a nadir of 1,800 with neutropenia (67.2% = 1200 PMN's). As the patient gradually defervesced (temp = 100 degrees F at 75 hours), the wbc count slowly ascended to 2,700 (PMN's = 2100) in spite of continued Claforan, The paralysis remitted over the initial 48 hours. concomitantly, the LFT's normalized rapidly, the Sjogren manifestations and cranial neuropathies disappeared, the BP became 120/70, muscle tenderness was reduced and the U/A was devoid of abnormalities.
By discharge to home on the 6th hospital day, the polyarthritis (as judged by joint swelling) had resolved in 75% of the involved joints and was ameliorated in the rest, and the fever = 99.6 degrees F. However, the knees were still painful and hobbled the patient, and range of motion was impaired in the knees, shoulders and hips. Biaxin, begun day 6, caused a transient acute memory loss from day 8-9 without fever.
Features supportive of the SLE diagnosis include: leukopenia, positive ANA, a high DS-DNA titer, arthritis (R/O erosions).
During the hospital stay, a more thoughtful insurance medical director rescinded an earlier prohibition for intravenous antibiotics. Had the first "reviewer" acceded to my initial plan of care, the paralysis and the hospitalization it prompted could have been avoided. Treatment is advancing. Repeat DS-DNA, ESR, ANA, CPK, C3, CH50, and X-Ray and MRI evaluation of joints is anticipated. The anemia is being investigated.
The tabulation of rheumatologic syndromes, either caused by LD or affiliated with it, is growing. Drs. Weber and Schwartzberg have reported Polymyalgia Rheumatica apparently caused by LD. As in the case above, Sjogren's Syndrome with LD has been published. Antibodies to Bb in the context of Psoriatic arthritis, systemic sclerosis and Reiter's Syndrome have been documented.
An expanding cohort of patients in my practice appear to have long-standing LD that dates to their "growth spurt" years and their past medical history contains the previous development of Osgood-Schlatter's Syndrome (water on the knee) in their teens. A relationship to LD can't be excluded.
Arthralgias and bone pain in LD can be excruciating. It is the imprudent clinician or parent who lackadaisically attributes these symptoms to "growing pains" or aging.
Another patient of mine recalled recurrent and migratory polyarthritis since he was 18 (1966). Monthly Medrol Dose Packs (steroids) failed to alter the clinical picture. In 1987, he was hospitalized with an acute exudative synovitis of the knee, whereupon ear lobe biopsy demonstrated the classic histologic feature of Relapsing Polychondritis, a very rare disorder with a peak onset in the 5th decade of life. In spite of continual high dose steroid treatment, (and later methotrexate with non-steroidal anti-inflammatory agents), he eventually developed a deforming arthropathy in his hands which progressed slowly between 6/90 to 12/92. Earlier physicians had discounted the significance of a positive Lyme Elisa = 1.09 in 4/91 as "low titer". An unsuspected encephalopathy betrayed its existence as memory and concentration impairment beginning 1/91. The patient presented for LD evaluation 1/93. Laboratory values include: an IgG by Elisa = 14.7, IgM by IFA = 80 and the Western Blot had bands at 31 and 41 KDA. the polysynovitis and encephalopathy proved rapidly responsive to antibiotics for LD. The patient was quickly emancipated from the other medications although steroids had to be slowly tapered and are now down to an inconsequential dose without recurrence of rheumatologic complications. The patient, although symptom free while on antibiotics, has permanent crippling deformities of the hands.
Cardiac complications arise in 8-12% of LD cases. Conduction defects and heart block, of which first-degree is the most common, can be discovered on EKG. A long rhythm strip should be employed to detect intermittent blocks. Higher degrees of heart block can result in fainting or death and may require cardiac pacemaker.
Sudden death can also result from arrythmias. Fast and slow heart rates occur, usually at the time of symptom flares, and sometimes in the manner of Sick Sinus Syndrome (tachy/brady). Ventricular tachycardia has been documented to attend LD infection in the heart, confirmed on cardiac biopsy. The cardiomyopathy may be complicated by congestive heart failure (CHF) as the following case might illustrate.
I had been treating a white male in his 60's for several years for LD with (initially IV antibiotics) oral antibiotics and in the main, his symptoms were controlled. However, he would occasionally complain of "traveling pains" (arthralgias). I was impressed with mild encepahalopathy (confusion) and he had a brief monoarticular arthritis of the right knee.
In concert with numerous consultants, our work up over a few years also uncovered: Diabetes mellitus (non-insulin dependent), COPD; hypertensive, ischemic and dilated cardiomyopathy (enlarged heart); both diabetic and hepatitis C related liver involvement confirmed on liver biopsy (not helped by a prior preference for alcohol); colon cancer for which he underwent a transverse colectomy (partial removal of the colon),colonic polyps; and Barrett's esophagus. A fall at work caused a LEFT sided appendix to rupture (talk about being thrown a curve?!).
Most significantly, he had been troubled with recurrent non-sustained ventricular tachycardia, atrial fibrillation and episodic CHF all of which increasingly escaped therapeutic control with the usual measures. This resulted in frequent hospitalizations, He had a small myocardial infarction of the diagonal branch in the past. A MUGA scan revealed an ejection fraction (a measure of cardiac output and pump function) of only 21% which is quite low. His exercise intolerance due to shortness of breath fluctuated but interfered substantially with his quality of life.
During a 1993 hospitalization for acute CHF compounded by ventricular arrythmias, we found that these problems were resisting attempts to completely regulate pharmacologically. In the past, I had noted that when his LD was flaring up, his cardiac status would deteriorate. As the patient had incurred Pulmonary Fibrosis (ultimately reversible) as a side effect of an antiarrythmic drug, he was not deemed a suitable candidate for cardiac biopsy.
Intravenous Claforan was begun empirically and to our astonishment, he recuperated from his CHF in short order. A repeat MUGA scan on day 5 of IV Claforan showed a NORMAL ejection fraction of 51%! This welcome and salutary change in status was maintained by prolonged IV therapy. On a program of continued oral antibiotics, CHF was controlled to such good effect that he was able to walk 5 miles in the dead of winter to my office without any shortness of breath or chest pain.
To my mind, one of the more remarkable aspects of this case was the disproportionate way in which cardiac complications dominated the clinical course relative to the other LD symptoms and yet all responded fortuitously to IV antibiotics. Thus treatment may not eradicate symptoms synchronously. The other salient lesson here is that he probably has CHRONIC LD, a diagnosis made purely on clinical grounds as serologies were always negative.
Again, differentiating Lyme cardiomyopathy from a mere exacerbation of cardiomyopathy (due to other causes) by LD remains an unresolved issue. Intuitively, we might suppose that the other component etiologies which contributed to his cardiomyopathy would not respond so briskly to antibiotics, unless there was an as yet undefined relationship with the LD. His cardiac and BP medications are now providing the customary benefits in a predictable fashion. On oral therapy alone, mild shortness of breath to stairs is once again emerging over time. Further evaluation is forthcoming.
Mitral valve prolapse is not uncommonly found in LD. MVP can be associated with confounding chest pain and ventricular arrythmias. It is often accompanied by Mg++ deficiency and LD can cause Mg++ levels to be low. In a few of my patients, MVP developed only after the onset of LD and resolved with LD treatment. Chest pain due to LD may arise from numerous causes: myocarditis, pericarditis, angina, asthma, bronchitis, periostitis of the ribs, pectoral myositis and tendinitis, sternoclavicular and costochondral arthritis, esophagitis and esophageal spasm, stomach acid reflux, and gastritis.
Elevated ACE (angiotensin converting enzyme) levels have been detected in LD (Leigner, 1990). The relationship between high ACE levels and heart disease may provide a mechanism to explain LD's anecdotally suspected tendency to accelerate Coronary Heart Disease and incite hypertension. Possibly, Syndrome X (angina with normal coronary arteries at catheterization) is due to LD induced arterial spasm, an event that might be enhanced by direct perivasculitis and/or Mg++ deficiency (see Grisold, M abstract No. 55F, V Int'l Lyme Symposium).
Potassium deficiency without an obvious origin irregularly evolves in LD. Rarely, the K+ losses are profound. This could be due to Mg++ deficiency. New onset or difficult to control hypertension is more likely to be seen. LD should be part of the evaluation of hypertension. LD treatment has permitted easy BP control in several patients, some of whom were able to forego using their traditional hypertension medications. Increasingly, I am encountering thyroid disease in LD. A local endocrinologist has remarked to me privately that the incidence of thyroid involvement in LD may be greater than expected from the normal population. A final judgement awaits formal statistical analysis. In many of these patients, the thyroid dysfunction was seen to originate in the pituitary or hypothalmus. Remaining alert to the possibility of thyroid disease is essential because there can be considerable clinical overlap with LD. Subacute thyroiditis is the most prevalent thyroid phenomenon I see in LD. Hypoadrenalism can uncommonly develop. Uncorrected hormonal aberrations can vitiate otherwise effective LD therapy. Like any infection, LD can provoke the onset of hyperglycemia and alter the facility with which diabetes is managed.
Impaired fertility and a loss of libido is not infrequent in LD. A reversible cause of infertility should be sought and ought to include LD. Reduced sexual interest without an ostensible justification is usually misinterpreted by the partner with predictable social and psychological turmoil. LD infection in the CNS or in the sex glands may be causal. In a few female LD patients, disturbed estrogen and progesterone levels were found. Early "menopause", skipped menses, and heavy menstrual flow represent a few of the perturbations in LD.
Women with symptomatic LD can experience new onset or heightened PMS (ballistic mood swings and irritability), or perimenstrual headache or cramps. The last of these theoretically could also be due to Pelvic LD infection (ooperitis or salpingitis) and/or elevated PGE-2 (prostaglandin E-2) levels, the latter having been reported in LD. A surfeit of PGE-2, free radicals, altered fat metabolism and general immunosuppression by LD may contribute to a predilection (stimulate or predispose) for oncogenesis (forming cancer). Carcinomas are not unknown in LD: melanoma, thyroid cancer, and lymphoma have been published. Free radicals, by engendering connective tissue cross-linking, could be responsible for intra-abdominal adhesions to form, and for some LD patients to appear older than their stated age, or have a haggard facial appearance.
Breast pain due to mastitis and testicular pain from orchitis have been described by some of my patients. So far, there are 3 men in our files whose chief complaint with LD was pelvic pain due to chronic prostatitis. The therapeutic strategems for LD provided superior relief whereas using Cipro or Doxycycline alone gave partial or temporary improvement.
Flawed studies have created the impression that pregnancy outcomes are not influenced by LD. There is substantial documentation to suggest a causal relationship between LD and stillbirths, congenital abnormalities, spontaneous abortion, low birth weight babies, prematurity and intrauterine fetal infection acquired from the mother. An outcome of untreated LD arising from Mg++ deficiency could be pre-eclampsia (hypertension) or eclampsia (hypertension with seizures). Magnesium is often relied on to treat these problems. Women with LD in pregnancy can experience severe morning sickness, gestational diabetes mellitus and prominent flares of Lyme related symptoms. As both LD and Sudden Infant Death Syndrome are attended by sleep apnea, this should impel further research to determine if some babies with SIDS are actually suffering from LD. Bb can appear in the breast milk.
Lyme patients very often complain of heel pain. This may be due to an underlying plantar fasciitis, with or without a heel spur, or periostitis of the heel. Epicondylitis (tennis elbow) is another complication. Carpal Tunnel Syndrome can also develop in untreated LD.
Lyme patients tend to heal slowly and are prone to musculoskeletal injuries, sometimes without the usual antecedents. One patient sustained a vertebral facet dislocation while shaving ( the usual context is athletic). Even in the well conditioned athlete, there can be an unexpected spate of muscle cramps, sprains, tendinitis and bone or joint pains at the sites of load bearing.
Muscle weakness occurs in some LD patients, More commonly, exertional performance is limited by shortness of breath, poor coordination, musculoskeletal discomfort, or fatigue. Exercise without or early in treatment can precipitate a flare of fatigue, especially the following day.
Low back ache can arise from sacroilitis, paravertebral lumbosacral muscle strain/spasm, and herniated vertebral discs. In a few patients, spinal stenosis is encountered.
Inflammation of the abdominal wall muscles, in particular the rectus abdominus is not an infrequent problem. Usually the tender sites are focal, involving more often than not, the lateral borders of the rectus abdominus muscle. Nausea is often present as well. The sites are best located when the patient is performing a Valsalva maneuver or doing a partial sit up. Failure to appreciate the abdominal myositis may lead to avoidable extensive GI workup.
A very helpful diagnostic maneuver is palpatory tenderness of the medial tibia shaft due to periostitis (inflammation of the tissue around the bone if not the bone itself). Periostitis is also common in another spirochetal disease, syphilis (Textbook of Medicine, Ed: Kelley, 1989, p. 1587) and is responsible for the bone pain that both syphlitic and Lyme patients experience. Tenderness is easily elicited in 95% or more of LD patients simply by pressing the bony aspect of the thumb joint against the medial aspect of the tibia about 3-6 inches above the ankle. The intensity of the pain experienced by the patient can vary, but is often exquisite and will cause the leg to recoil abruptly. The pain often lingers after this procedure. In a minority of LD cases, periostitis is generalized and I have appreciated skull involvement in a few instances. A small proportion of LD patients have periostitis.
As a result of fibrositis, myositis, periostitis, is it any wonder that the ill LD patient view hugs as potential torment? The chagrin of mystified family members is understandable. Self-examination for periostitis can be unreliable. Periostitis pubis (of the pubic bone) can mimic bladder pain or be the origin of lower midline abdominal pain, especially in children.
Lyme (and Brucella) should be included in the differential diagnosis of Desert Storm Syndrome, with which LD shares many features.
The abundant research opportunities should be clear to all. It is unnecessary to give Lyme Disease the "Galileo" treatment. Thank you for your interest. Comments and criticisms are welcome. The End.