Hi, I haven't been on this site for few yrs..I have another article of Dr. Bleiweiss..When I first read it I thought it was goofy..But I later found out due to my symptoms and my husband's - he is 100% correct..absolutely. As both of us had some of the
weird and uncommon symptoms he notes plus typical ones.

I think I saw Dr. Bleiweiss wanted have a book of his published and the evil Drs. of the other side put a damper on it.


On Sunday, November 24, 1996 at 3:00:00 AM UTC-5, rita...@aol.com wrote:

WHEN TO SUSPECT LYME DISEASE
John D. Bleiweiss, MD
Trenton, NJ 4/94

Traditionally, the public has been advised to suspect Lyme (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 variey 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 (eg. 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 WW II, 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 inoculation 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 (Ploymerase Chain 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 autoimmune 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 microbiologically contracting the disease. Arthritis(ie., joint inflammation; distinct from arthralgias; ie., 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 symptoms 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 of professional imperatives to presumptuouusly 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 exacerabtion 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 persperation or sleepiness. Photophobia can enhance the somnolent propensity that can occur while
driving a car. Significant head trama 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 inaccuraaacy 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 privatecommunication, a physician reelated 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 4
PM, whereupon a short nap provides refreshment. "Madman Syndrome"
(explosive irritability) may appear toward the end of 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 diagnosses 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 be consicered.

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
fanges 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: Kelly, 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. Attemptss to indulge avocational or vocational pursuitsis frequently interdicted by either the languor of Lyme or by encephalopathy. There is a tendancy 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 obes are varying shades of red. Less commonly, a similar erythemma 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 inthe 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 ofhyperthyroidism. Oneof my patients experience 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 the "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, whereobjects were placed, the
previous sentence or plot content,calendar dates, teir schedules, names
and faces of familiar people, even family members. Cognitive neglect
caused one patient to wander around the room looking for the room looking
for the pencil clenched between his teeth. A mother left her infant and
baby carriage in my office parking lot and went home. Others forgot 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 initial 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, bypawwing 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. numericalerrors are common. Sequential task performance is compromised in Lyme. Lyme patients have a penchant for saying, "Waut 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
amoung the myriad cognitive flaws are the frequent errors of word
selectionor 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 (Obessive Compulsive Disorder). These clinical features all remitted with
antibiotics! A real estate agent's prominent encephalopathy resolved with
LD treatment whereupon his commercial outputjumped 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
spels 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, super critical dispositions, and impatience with themselves or others. Lyme patients can be easily irritated by anyone just walking into the same room weven 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.

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