Lovie pm'd me asking me if I had ruled out Lyme disease. I was tested for it several times, always negative but Lovie motivated me to do more research. Lyme disease tests false negative frequently. Reading more - many people with Lyme disease get dx with ra. Now I am really fascinated. I read all the symptoms and they match my symptoms. So now I am going to go back to my gp and see if he can give me a good argument that I was not misdiagnosed. The only thing that has never matched up to ra is I do not have the morning symptoms. My symptoms get worse through out the day. If I have Lyme disease, I should be on antibiotics. So, if you spend a lot of time outdoors as I do, you may read up on Lyme Disease. I get several ticks every year! Hey you guys. If I do have Lyme Disease. Can I come back here and visit you When I first got sick they thought it was Lymes disease cuz of a mark I
had on my stomach. We lived in Indiana at the time. More testing showed
a collegen disease, then finally RA...it took several blood tests to
show it was RA.
Could be LD...worth a check anyway.
Roxy- when do you take your prednisone? I was waking up in alot of pain so i decided to take it at night that way i dont wake up stiff and in pain and when i am in pain at night before the prednisone kicks in im home and its not necessary i run around like i do in the morning. It works well for me, if its not lymes disease it might be something to think about.. Just a suggestion
Make sure to mention that certain test my friend talked about. She was tested about three times before this one particular test gave them the proper dx.
Treatment is kind of the same. She is on antibiotics; but she's also using Humira. That's good news considering you've already been approved.
The thing that makes me so curious about this in your case is that after all of this time none of the treatments you've tried are making much of a difference...except predisone. That's exactly what she said.
Knowledge is power sister...sometimes these doctors need a little help to think things through. A lot of doctors welcome our input; some do not. Find one that's willing to listen to your concerns.
Let us know how we can help.
Lovie
Big hug to you Lovie. It is definitely something I am going to look into. We are going to the mountains for the day. I will check in with you guys later. Have a great day.They tested me for Lyme disease before being diagnosed,they say Lyme disease acts just like Ra in the joints,but I guess you can get a bulls eye looking rash with Lyme disease also,they just did blood work to test me for it and also looked my body over for any rash.If you had that maybe you have hope to be OK again,it;s worth a try exspecially being outdoors and the ticks,good luck,sherry
You need to ask your GP to do Western Blot. If your GP does not understand how to interpret the result. ID (infectious disease) doctor can do that for you. I had 41 KD and 66 KD “reactive” result Here’s what my ID dr. told me. “This is a negative result. IgM (indicative of acute disease) are all negative, IgG (indicative of chronic or previous disease) show only 2 of 10 tested bands positive. These are, BTW, the most commonly "false" positive bands. If you have an autoimmune disease (as it appears) even the IgM are often false positive but in your case the test is negative for active, acute or chronic Lyme.
So April, If I print out your post, will my gp understand it? I am going to make an appt. today. I am hoping it is Lyme Disease. Seems like a better dx especially since rd talks about my rd being "aggressive". I think I like the treatment anyway. ANTIBIOTICS. Feels less scary. I always respond well to antibiotics. Thanks you guys. I am going to look into it.
How are you feeling? I hope better. I think I am starting Humira soon Lovie. I pray I have the same results as you and I will say a prayer that you get to get back on your meds soon.
I have an appt. on MOnday to check into Lyme disease. I hope you are having a good day and thanks for checking on me
Your GP should know about the Western Blot test. My ID dr. told me that there was no Lyme in my area but I wanted to have Lyme disease so badly and had the test done. At least, now I know for sure I don’t have it. RA will be my life time mate.
Good luck!
Still coughing some; but I really think I'm on the mend this time. The new antibiotic and the predisone seem to be working. Hopefully I'll be through this and back on my meds by next weekend. Starting to have asorted RA related pain; but the predisone is helping with that and i've been using pain meds, muscle relaxers.....and this super cough medicine with codine that really helps me especially at night!! Keep your fingers crossed for me.
I'll be anxious to hear what the doctor thinks about this new information you have to talk to him about. It's worth a shot!!
Get some rest.
Lovie
roxy, hopefully after you start Humira you won't have the "day after aches" anymore. After a little yardwork the aches the day after were keeping me on the couch resting ...but now I can go work outside for a few hours and not have the day afters! Glad you are feeling better Lovie! Murph, I would soooooo love to have more good days than bad. I am feeling more patient after having a good one though. Thank God I have some good days. I don't think I am as strong as so many on here. I need to feel my old self sometimes and I thank God I do. It breaks my heart reading some of these posts. You have to be tough to have RA !!!!! Lovie, it is good to hear you are better. You are my light at the end of tunnel !Patience is definatley required with this disease. I have an uncle with really bad RA..he can't tolerate any of the drugs. He tried MTX and couldn't stop throwing up. He is almost bedridden from the disease. It's hard for me to talk to him since nothing works for him, and the drugs work for me.Hey Roxy,
YOU BETTER NOT LEAVE US!
Shawnie
Thanks Shawnie. I am going to print out all the info I got from Lovie and Murph and bring it to gp. I got an appt. on Monday. I am going to demand I get another test. The two things I wonder about are: I don't have the morning stiffness and I seem to ALWAYS have a sore throat. That doesn't sound like ra does it? I wouldn't ask my rd. Last time I was there I asked him if he was certain I have ra. He was very stern and said that "there is no doubt about it". So he is not open to other possibilities. It is worth a try.
PS I would come back and teach you guys every thing you didn't want to know about Lyme Disease if I did. I would miss you guys too much but who would FAKE RA
That would be better news than ra. How did you get to be a senior member, I'm still a newbie. Ha.
I've missed this place, computer problems. Don't leave us, Roxy!
Mailady
Hey Mailady, Its called being home on disability and no energy but to sit and yack on the computer with all the great people on this site that actually understand how I am feeling. Good to see you back.I was diagnosed with MS in Jan 2005. I tested negative for lyme disease. I am 50. That is pretty late to be diagnosed with MS.
Several people have told me to get re tested for Lyme. The one gentleman told me his friend was diagnosed with MS 10 years ago and it was Lyme disease. He says I walk just like him. Here are my symptoms spasticity in legs only with no pain associated with it...when I get any type of anxiety, my legs stiffen up and I look like a tin man. It is like jolt and my legs just stiffen up. The only other symptom is some weakness in my right side. Anyone ever experience this type of symptom with the stiff legs?
Thanks
Hi,Thanks Ron. I had several tests for Lyme, all of the tests available. It would have made sense as much time as I spend outdoors. I also get ticks a few times a year feasting on me. I am definitely negative for Lyme and very positive for RA. Who would think you would WANT a disease, but my life would be way better right now if it were Lyme. I haven't lost my job yet and thanks for understanding. I am going to fight it to the end. Our union rep. is out of town this week so I will hopefully have some news when I talk to him. I am sorry you lost your job. I am not ready to lose the income or the rewards of going to work to a job that makes me feel so blessed.
It is hard for me to consider doing anything else. I am 50 years old. I can't sit at a desk. It makes me crazy - that is why I have a laptop Let us know how things go with your job. I really hope it goes your way. There are so many of us that could be in your shoes at any moment. I hope it works out so that you can get back to your job feeling better. Thanks Arizona and everyone.
Hi Roxy,
I have been off line for the past few days. Doing research about my conditions. It is very interesting that this post was on when I came back. I also suffer from sore throats quit often, along with mornings stiffness that lasts sometimes all day, sleeping patterns are horrible, joint and bone pains, sometimes very sudden sharp pains that travel ( this could be lymphodic ? ) not sure, nodules on elbow and on cervical spine, swelling and pain in feet, hands, and sever headaches, sensitive to light, memory conditions, and other various problems. While researching I came across an article on EBV and Infectious mono, it also speaks about RA and related symptoms. Here is the link http://www.emedicine.com/med/byname/infectious-mononucleosis .htm , this is a good site for information on just about everything, something else pretty neat, while you are reading and need to look up something just highlight it and it will pull up another box and give an explaination.
Just hope you find out what is going on, Good luck. Sharon
it is not a big deal. you do can go back to normal. be well.Traditionally, the public has been advised to suspect Lyme disease (LD) if a round or oval, expanding, red rash develops 3-32 days after a deer tick bite associated with or followed by a flu-like illness. This limited description will apply to only some cases. About 50% of patients do not recall one or more of tick bite, rash or flu-like illness. The rashes associated with LD can assume a variety of morphologies including vesicular, urticarial, eczematoid or atrophic (Acrodermatitis Chronicum Atrophicans). For many patients, neurologic, cardiac, arthritic, cognitive and/or psychological complications predominate. While deer ticks and LD have a well known affiliation, other potential vectors can carry the spirochete that causes LD (Borrelia burgdorferi; Bb). These include, the lone star tick, fleas, the biting flies (eq. green-headed fly) (and mosquitos?) A case of suspected transmission via blood transfusion has been reported by Dr. Burrascano.
The demonstration of Bb by PCR in two museum mouse specimens dating from 1894 Massachusetts) and in ticks collected during WWII provides a mechanism for potential life long exposure and disease which predates the formal 1975 discovery of LD. An occasional patient will date their symptoms which resolved on antibiotic therapy for LD to early childhood. Before the diagnosis was made, patients would dismiss those symptoms with the statement: "I've always had those problems". That resigned characterization implies that the longevity of the symptoms rules out a reversible cause. Subsequent resolution of the long standing symptoms on antibiotic therapy for LD belies that notion. Symptoms of LD can begin within days of innoculation with Bb or appear belatedly, but usually in the first to fourth month. Mice innoculated intraperitoneally had Bb demonstrated in the brain on biopsy 12 hours later with a peak at 48 hours (Stockholm Conference, 1990). Dr. Luft has published the detection of Bb by PCR (polymerase Chn Reaction) in the CSF (Cerebrospinal fluid) of humans 2 weeks after the appearance of non-CNS related symptoms!
If dissemination can occur early, then staging the disease according to the temporal appearance of symptoms may be irrelevant. The absence of symptoms related to a particular organ system doesn't necessarily exclude the presence of Bb from that organ. Conversely, due to the possibility of symptoms being engendered by chemical mediators and autoimmunue reactions by the host (against non-viable but immunoreactive DNA blebs), organ dysfunction and attendant symptoms can appear at sites removed from the actual spirochetes. The diagnostic and therapeutic problems that these phenomenon entail should be obvious.
Rapid dispersion of Bb could lead to the prompt appearance of complications, eg. meningitis. There is no absolutely predictable clinical sequence for LD.The flu-like syndrome may be absent from the initial presentation and may endure once established without treatment. Cardiac and neurologic complications can be observed sometime within the first 3 months after the disease. Arthritis, (ie. joint inflammation; distinct from arthralgias, i.e. joint pain), can also accompany the initial clinical course, but more often develops later on between the second and sixth month from innoculation. The onset of complaints can not only be subtle and desultory, but delayed for a year or more. One of my patients denied all LD related symptoms until her husband died, whereupon a plethora of complaints cascaded into her life beginning that very day. Another had an annual flare of LD as part of an anniversary reaction centered on the date of his mother's death.
Moreover, the early constellation of symptoms can have a paucity of findings with unidimensional presentations: the onset of solitary problems such as vertigo, or recurrent upper respiratory tract infections. Over time, as the untreated LD percolates, symptoms accrue to the burgeoning clinical picture until a multisystem presentation is created. Other patients can have their manifold symptom complex develop in the manner of an avalanche. These patterns represent the extremes of a clinical continuum between which there are many variations on the theme ranging from mild to severe disease. Thus, the failure of a pathognomonic (unique and specific) presentation to consistently unfold causes sufficient clinical confusion, that a punctual diagnosis is problematic. Therefore a high index of suspicion is placed at a premium. If a clinician can't reconcile preconceived notions about how LD should announce itself with a patient,s history and physical findings, it is a disservice to the patient and an abdication professional imperatives to presumptuously conclude that the symptoms are psychosomatic or that the patient is faking!
Antecedant or concommitant factors which can cause symptoms and physical changes de novo or aggravate contemporary problems are reliably solicited on close questioning of LD patients. Females experience an exacerbation of their LD symptoms before or during their menses, while pregnant and with oral contraceptive hormones. Many patients have symptoms intensify or reappear with physical and emotional stress, if sleep deprived, after exercise, in a hot bath, after alcohol consumption, with fasting (hypoglycemia) or dehydration. Humidity, low barometric pressure, cold or rainy weather can elicit arthralgias, fatigue encephalopathy or headache. A cold draft of air can precipitate the appearance of pain in exposed skin and the underlying bone, or even VII cranial nerve (Bell's) palsy. Patients with poor control of symptoms abhor the extremes of ambient temperature. Typically, heat intolerance is revealed as irritability, headache, excessive perspiration or sleepiness. Photophobia can enhance the somnolent pronsity that can occur while driving a car. Significant head trauma has incited severe symptoms that later resolved with antibiotic therapy for LD. A sudden acceleration of encephalopathy (see below), headache and dizziness, thought of as putative post-concussion syndrome, can be evoked by head trauma. Diagnostic inaccuracy will be minimized by not indolently attributing all problems following head trauma to the most obvious cause. I routinely advise my patients with LD to abstain from cigarettes, alcohol and steroids because therapeutic inadequacy or an avoidably prolonged convalescence is frequent (Dattwyler RJ, Lancet 1:687, 1987-on steroid use). Patients have described clinical deterioration when steroids were used fortuitously or intentionally when hypoadrenalism was absent. Another hazard attending palliative steroid use is that some symptoms will be concealed, rendering the clinical picture less interpretable. In a private communication, a physician related that one of his LD patients succumbed to FATAL cardiomyopathy after receiving steroids. One helpful caveat is to avoid the use of electric blankets or sleeping in water beds with the electric current activated, otherwise you might wake up with one or more LD symptoms. Allergic and chemical hypersensitivities can enhance or cause symptoms to emerge temporarily.
Symptoms vary stereotypically during the day. Joint stiffness and "brain fog" are often reported on rising in the am (but not solely in the am). Fatigue can be unrelieved by sleep, or develop between noon and 4pm, whereupon a short nap provides refreshment. 'Madman Syndrome" (explosive irritability) may appear toward the end of a stressful work period or late in the evening. A "mad face" can herald imminent detonation.
Prior to proper diagnosis, patients habitually report that they were assigned the following diagnoses most often: Chronic Fatigue Syndrome, Multiple Sclerosis, Fibromyalgia, Lupus, Candidiasis, Chronic Mononucleosis, Hypoglycemia and Stress-related illness. If these appear in a differential diagnosis, then LD should also be considered.
On cursory inspection, many patients with LD appear deceptively well but in fact feel awful. Don't be fooled! The mien of a Lyme patient ranges from phlegmatic, sullen, staring off into space, to one of agitated anxiety and hyperkineticism. Their oral and written recitations similarly vary from cryptic to being overinclusive and circumstantial. Geschwind's Syndrome embraces some varieties of LD encephalopathy precisely (Textbook of Internal Medicine, Ed: Kelley, 1989, p. 2509). Stuttering was reported by several patients to coincide with the onset of their LD and often proved reversible.
Patients most frequently report fatigue that varies from mild to debilitating. Usually there is a loss of interest and initiative so that lounging around becomes habitual. This derives not from laziness, but results from lassitude. Attempts to indulge avocational or vocational pursuits is frequently interdicted by either the languor of Lyme or by encephalopathy. There is a tendency to nap, sleep that is not rejuvenating, and hypersomnolence at inopportune moments- eg. in the classroom or during a favorite pastime. Sleeping away entire days is not unknown. Paradoxically, at usual bedtimes, patients often experience insomnia or frequent awakenings. Sleep does not always provide respite as ferocious or vivid nightmares can occur. Childhood night terrors can be due to LD or more mundane causes.
Intermittent fevers range from low grade to 104.5 degrees F. The typical context for high fevers is in the first week of antibiotic therapy, especially if multiple agents and/or IV drugs are used. While fever is the hallmark of the classic Jarish-Herxheimer (J-H) reaction, its appearance is inconstant. Compared with most causes of high fever, the patient can look and feel their best during or shortly after the fever with a relatively non-toxic demeanor. This can sometimes be diagnostically helpful. The differential diagnosis of febrile seizures in infants should include LD. Many LD patients have routinely subnormal body temperatures so that the appearance of a temperature of 98.6 degrees F may be compatible with a low grade fever analagous to diabetics.
Very often, the pinna and ear lobes are varying shades of red. Less commonly, a similar erythema can be observed on the hands or malar (upper cheeks) areas. A malar rash is not pathognomonic of Lupus, if in fact SLE is distinct from LD (Abstract 55A, V LD Symposium). Fifth Disease (slapped face) is suspected of being due to LD. Lymphocytoma of the ear lobes has been encountered more often in Europe. Cold hands and feet even in warm environments occurs and some patients have Raynaud's phenomenon. Potentially contributing to this vasoconstriction are excessive levels of vasoconstricting hormones, magnesium and potassium deficiency, limbic or hypothalamic dysfunction due to CNS infection, local inflammation of capillary sphinctors or hypothyroidism. Eczema and psoriasis can appear in conjunction with LD. A female LD patient had generalized psoriasis covering 40% of her body. Antibiotics for LD gave total relief.
Alterations of cutaneous sensation are very common. Most often there is numbness and tingling (paraesthesias) of the central face, fingertips, scalp and in the extremities. Muscle twitching usually occurs in the eyelids and extremities. Tremors, myoclonic jerking of entire extremities or truncal shudders can suggest pseudoseizures but is attributed to neuritis. Patients also report electric shocks, dysesthesias (abnormal sensory responses to stimuli), painful or itchy skin and flushing. An inordinate amount of exertional or non-exertional sweating may be described in the absence of hyperthyroidism. One of my patients experienced anhydrosis (inability to sweat) for 27 years until antibiotics were given for LD.
Dizziness, imbalance and clumsiness can become very frustrating as patients drop objects or knock them over, trip alot, turn into the wall when rounding corners, and develop sloppy and slower handwriting.
Many use the phrase "a vibration in my head". Others remark that they feel "toxic". Along with "brain fog", these colloquialisms connote LD until proven otherwise.
Eventually the majority, but not all, complain of one or more of "foggy brain", forgetfulness, anxiety, mood swings, loss of initiative, depression, impairment of concentration, inattention, easy confusion or disorientation when attempting intellectual tasks. Paper shuffling can be the end result when patients attempt to organize or assimilate even limited amounts of information. These problems, and the others described below, constitute the salient features of Lyme encephalopathy.
Short term memory impairment causes patients to forget what they were going to say, why they entered a room, where objects were placed, the previous sentence or plot content, calander dates, their schedules, names and faces of familiar people, even family members - cognitive neglect caused one patient to wander around the room looking for the pencil clenched between his teeth. Another left her infant and baby carriage in my office parking lot and went home. Others forget how to spell even simple words, how to read or must re-read with varying degrees of comprehension. One patient drove to Philadelphia instead of the desired Princton destination because the intial letters were identical and confused him. After shopping for groceries, another patient placed her shoes in the refrigerator and stored the food in the clothes closet. Lyme patients can loose their way home or on the way to work, bypassing otherwise familiar exits or plain forgetting where they are in time and space or how they got there.This is known as topographical disorientation or environmental agnosia. Elementary math problems may prove insurrmountable. Numerical errors are common. Sequential task performance is compromised in Lyme. Lyme patients have a penchant for saying "wait a minute" 2-3 times rapidly when the only demand on them is to record a phone number, which also speaks of perseveration.
Inattention frequently characterizes the way patients relate to the world. Some patients participate passively, unable to initiate or engage in the usual forms of social and intellectual exchange. Verbal and written forms of expression have a typical Lyme flavor. The content demonstrates disorganization, an inability to follow a train of thought and there is a proclivity to ramble on and on in great detail which propels further confusion amongst the forest of details. Ubiquitous among the myriad cognitive flaws are the frequent errors of word selection or pronunciation and the consistent word and number reversals.
Concentration on a task can be problematic because attention span is abbreviated. As increasing amounts of information have to be processed, the Lyme patient becomes proportionally lost, disoriented, frustrated, fatigued and finally must desist from further intellectual activity. The desire to initiate projects and social interaction is often blunted if not absent altogether. Thus a deterioration in academic and vocational performance is a frequent manifestation of LD in children and adults.
Miklossy (NeuroReport 4: 841-848, 1993) reported the detection of Bb spirochetes on darkfield microscopic examination of post-mortem brain biopsy specimens FROM PATIENTS WITH ALZHEIMERS DISEASE! CSF and blood cultures grew out Bb from those cases. In my view, a child assigned a diagnosis of Attention Deficit Hyperactivity Syndrome (ADH) or PNI (Perceptual Neurologic Impairment) should be evaluated for LD. A 16 year old boy whose Tourette's Syndrome began at age 5, had Osp A antigen detected in his CSF. LD treatment resolved the Tourette manifestations. Another patient of mine with ADh had a positive IgM Lyme antibody in the serum. The manifestations of ADH were eradicated while on antibiotics. Distinguishing causality from mere exacerbation of ADH or Tourette by Lyme is moot and therefore I suggest an evaluation LD for these patients. Parenthetically, the boy with Tourette also had cognitive impairment, familial nephritis with early renal insufficiency and OCD (obsessive compulsive disorder). These clical features all remitted with antibiotics! A real estate agent's prominent encephalopathy resolved with LD treatment whereupon his commercial output jumped to a record zenith and became the recipient of numerous corporate awards. The benefits of arresting LD are self evident to him.
Personality changes are nearly universal in Lyme encephalopathy with emotional and expressive incontinence being typical. Usually there is a baseline irritability which fluctuates. Patients with LD encephalopathy react to even mild degrees of stress with frustration, anger or crying spells out of proportion to the situation. Emotions can reach escape velocity and rages can become volcanic with a momentum beyond volitional control. Unpleasantness is inevitable due to volatile tempers, supercritical dispositions and impatience with themselves or others. Lyme patients can be easily irritated by anyone just walking into the same room even though eye contact is never made or words exchanged. Low threshold exasperation in unexpected circumstances is not uncommon. Thus a parent responds to an infant's needs with anger and frustration. Perpetrators of "shaken baby syndrome" recapitulate an emotional response indistinguishable from that of a Lyme patient whose encephalopathy is out of control.
Many express morbid fears of occult illness, impending death and can be generally pessimistic or maudlin. Some develop intricate paranoid theories regarding imagined conspiracies against them. Lyme patients often evince a tendency for being overly sentimental. Hyperbolic thought finds expression in obstinacy, self-righteousness, being contentious, speaking in categoricals and inappropriate and atypical vulgarity. Internalized anxiety results in the perception of being hurried even without a deadline or the inability to remain calm when there is no reason for not feeling calm. Panic attacks are the extreme of this anxious state and should arouse a suspicion of LD. I suspect that in addition to ONS infection of the lirribic system, these phenomenon could also be the result of elevated adrenaline levels, Mg++ deficiency or hypoglycemia. A rare LD patient will admit to agoraphobia or claustrophobia.
Depression alternating with anxiety is very common in LD. Psychiatrists should routinely evaluate a depressed patient for LD before/when initiating psychotropic medication. A patient with LD may have a plausible reason to be depressed, but their emotional response can not only be incongruous with their usual coping style but also the depression can be ablated or ameliorated with control of the LD infection. Lyme encephalopathy typically vitiates an otherwise mature and functional emotional repertoire.
With a loss of voluntary and subconscious editorial control of emotions and expression in word or behavior, a patient with encephalopathy gives the general impression of being erratic, inappropriate, if not dysfunctional. Less frequently, mania, obsessive-compulsiveness, schizoaftective disorders and homocidal/suicidal ideation is encountered and has been reported. Fatal attractions are consistent with the LD style.
Adolescent hormonal surges and the emotional turmoil wrought by LD at once camouflage and exacerbate each other mutually. Thus, children tend to be unruly, hard to please and prone to atypical emotional reations. A child who is misbehaving in class should not be dismissed as a "bad kid". Lyme can catalize inappropriate behavior and commentary. Many patients retrospectively realize that they were out of control but in the event were unable to intercept their behavior. Misattribution as to the origin of behavioral perturbations is the rule. The development of aberrant personality traits can be gradual or even situational, further obscuring the medical etiology. An acute break from normal behavior can serve to highlight the abnormalities and suggest the need for evaluation. Thus, dysfunctional behavior and intellectual incapacitation are bitterly recalled by LD patients when they finally realize how their interpersonal relationships, school and vocational conduct were negatively impacted.
Clinically, there is considerable overlap between LD and Chronic Fatigue Syndrome (CFS). In their masterful review of the pathophysiology of CFS, Drs. Rosenbaum and Susser (Solving the Puzzle of Cys, 1992) describe SPECT scan findings of brain perfusion (blood flow) in CFS patients. Hypoperfusion of the left temporal, right parietal and left frontal lobes were consistently seen. These regions control the very areas of functioning which are abnormal in both LD and CFS, namely verbal capacity, memory, emotions and higher order information processing. Dr. Jay Goldstein has proposed the term "limbic encephalopathy" to describe the disorders of memory, appetite, temperature and appetite regulation, libido and hormonal homeostasis seen in CFS. He advances the concept of an "agent x" which incites CFS and causes dysregulation of the immune system and the limbic components of the CNS. I feel "agent X" is Bb. I am encouraged in this view by anecdotal experience whereby CFS responded to antibiotics given eitherortuitously or by way of Lyme treatment, due to positive serologies (antibody tests) for LD in some CFS patients and the development of a J-H reaction in CFS patients who take antibiotics. Crimson crescents, portrayed as diagnostic for CFS, I have detected in LD where the diagnosis was secure.
Limbic encephalopathy elegantly embraces the preceeding observations in Lyme encephalopathy. It is a potential mechanism to explain my suggestion that LD can be responsible for anorexia nervosa/bulimia. Anorexia was documented in earlier studies on LD. Uncinate fits and are characterized by hypersexuality, rage states and vulgarity, are compatible with LD. Indeed, disinhibition, the release of the usual brakes an behavior, would be part of limbic dysfunction.
LD could cause reversible disturbances in brain physiology through cytokine mediators, direct infection eg. encephalitis and perivasculitis, demyelination, metabolic abberations within theCNS 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 and 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 MS literature in Medical Hypothesis (vol. 25: 89-92, 1988) and advances the notion that LD is causing MS! His survey revealed that multipie studies prior to 1951 were able to demonstrate spirochetes in the spinal fluid of MS patients (by innoculation 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 Gherig'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 Ophthalmol 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 trigeminnal neuritis. Rule out dental abscess or sinusitis which can present with similar tooth pain.