jwissmille

".... There is no absolutely predictable clinical
sequence for LD.."

"....... 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!.."

"........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...."

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\0
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 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


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. Attempts to indulge avocational or vocational
pursuiis 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 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 ofhyperthyroidism. 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 a lot, 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
lose their way home or on the way to work, by passing 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 amoung 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 (Obessive Compulsive Disorder). These clinical
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, 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 .

jwissmille

".... There is no absolutely predictable clinical
sequence for LD.."

"....... 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!.."

"........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...."

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\0
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 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


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. Attempts to indulge avocational or vocational
pursuiis 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 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 ofhyperthyroidism. 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 a lot, 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
lose their way home or on the way to work, by passing 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 amoung 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 (Obessive Compulsive Disorder). These clinical
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, 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 .