Lyme Medical Workup
by
Harold Smith <haroldsm@sunlink.net>
Summary: the medical workup (labs, etc.) to rule out Lyme disease
(and its relatives).
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Some won't diagnose neuroborreliosis without a positive spinal tap. Others
make the diagnosis clinically.
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Spinal tap results are particularly helpful if the criteria one uses is
directed at helping the patient by being able to report the disease to
the Center for Disease Control.
-
If one's emphasis is directed at being able to help the patient foremost,
then positive spinal tap results may be less rewarding.
(remember it is the same criteria for the spinal fluid as for the serum
i.e. a positive ELISAtest and Western
Blot on spinal fluid after adjusting for differences in fluid composition)
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These tests may be more helpful in the first three months of neuroborreliosis
when there is more often an active meningitis
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with 100 to 3000 white blood cells predominantly lymphocytes and monocytes,
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elevated opening pressures and
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occasionally elevated protein.
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sugar is normal.
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thus the typical picture of a "viral" meningitis.
More often absent are the clinical signs of
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fever,
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positive brudzinski test or
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babinski,
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maximum headache level,
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emesis, and
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cortical confusion or
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somnolence,
thus misdirecting the unsuspecting physician.
More often it is just
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headache,
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some stiff neck or spasms, and
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perhaps other cns abnormalities such as autonomic dysregulation.
As borrelia
-
moves away from meninges into perivascular sites in the brain stem,
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moves intracellular and
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alters its form to wall deficient or membrane wall-less forms (which continue
to replicate),
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modulates its outersurface protein expressions and
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takes on wall membranes from host cells,
there is
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less and less immune response and meningeal inflammation and
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more of a basilar brain chronic dysfunction.
Brorson's
work demonstrates that spinal fluid induces motile Bb spirochetes to
transform into these bleb or larger cyst forms without identifying walls.
This may explain Andrew Pachner's observation ( JAMA symposium on LD
in 1995) that he often finds POSITIVE PCR DNA spinal fluid in neuroborreliosis
patients who are NEGATIVE by ELISA and Western Blot in serum and spinal
fluid ( at least negative for reporting criteria- maybe they are positive
by specific bands such as 23 (OspC), 31
(OspA), 34 (OspB)).
Thus the doctors could do
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a spinal tap for PCR DNA,
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antibody responses, and even a
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BSK culture ( which the FDA recs should not be replaced by antibody testing,
but few university centers offer the test).
There are other tests that could detect CNS dysfunction besides the spinal
fluid analysis.
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PCRs can be done on any monocyte layers from spinning down the csf- but
this is done at a research level.
-
Variant form culturing of csf might be the right direction to find Brorson's
blebs. This is on hold. No one in high places wants to believe it.
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However, SPECT scans do have a high yield (50%) and
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MRIs enhanced have some yield (an MS like pattern) especially if there
are brain stem hard focal findings on exam).
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A sleep study can demonstrate failure to enter deep REM levels.
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Tests of neuroendocrine dysfunction can be done such as TSH response to
TRH ( can be extremely high or nothing),
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ACTH stimulation of cortisol (no change), or
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Human Growth Hormone response to GH releasing factor. It is expected that
the autonomic dysregulation from central nervous system disease would often
be reflected in abnormal regulatory responses not detected by systemic
TSH baseline or cortisol baseline static testing.
-
Advanced neurocognitive testing can be done (about 2500 dollars around
here) which appears to yield little more than impaired organizational memory
in many victims.
All in all, neuroborreliosis, being predominantly
-
a subacute encephalopathy secondary to chronic basilar vasculitis and perivasculitis,
-
circulating cytokines and neurotoxins (with a somewhat anticholingergic
like pattern),
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demylination or disruption of white matter interbrain stem pathways, and
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perhaps autoimmune attack upon synapse receptor sites
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mixed in with neuroendocrine dysregulation,
- all this results in little yield from csf studies in later neuroborreliosis.
A more reasonable approach all said is perhaps doing
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Western Blots on serum IgG and IgM looking for specific band patterns supportive
of Bb infection systemically ( as reported by Bingnam in 1992),
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urine antigens for specific wall fragments at IGENEX,
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a buffy coat acridine orange stain for motile spirochetes concentrated
in the cellular layer,
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a detailed neurological exam and history for cranial nerve dysfunction
beyond Bell's palsy, and
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a brain SPECT scan.
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PCR on
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serum,
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urine,
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spinal fluid or
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skin sites
of chronic Borrelia infection manifestations may be rewarding but appear
somewhat insensitive as first level testing.
Regarding the differential diagnosis- Dr. Bransfield listed a source by
Dr. ?Weiss of the other infections that can cause a similar chronic subacute
encephalopathy with other disseminated organ features. I haven't found
it yet.
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VDRL,
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AIDS,
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Toxoplasmosis,
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cytomegalovirus,
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and things like mad cows
come to mind, but I'm still in the barnyard about what organisms to search
for.
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Thyroid profile is fundamental but flawed.
One word in parting,
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chronic disseminated Borreliosis often causes a persistent blood picture
of 8-12 % circulating monocytosis (an increased amount) which looks just
like mononucleosis.
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EBV virus studies for active infection status might be helpful when negative.
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(Paul Duray 20 years ago described in his writings that Lyme Disease masquerades
as mono. Monocytes have the duty of eating large microbes such as Borrelia
and arise from stimulating stem cells in the marrow. Unfortunately for
us, Borrelia can coil and live in the monocytes without being destroyed.
Kind of like the enemy's aircraft sharing tie down spots on our own aircraft
carriers.
IgM should be done as well as IgG since IgM is constantly stimulated
by new antigen expressions from the same and new generations of
Bb.
Urine antigen (LUAT) at IGENEX
often inversely parallels the Western Blot results
-
since it measures free specific antigen it will be high when the
free specific antibody is low or not detectable.
Since antigen and antibody are complexed during this disease it is only
when one or the other is in excess and free from complexes that their presence
in the free form can be detected.
-
Since the antibodies are polyvalent, it can require a large load of excess
borrelia antigen to be measurable independent of the complexes.
Steve Schutzer demonstrated this fact 10
years ago and repeated it recently in JAMA.
Still no one tests the complexes in precipitated samples as it should be
done from his work.
ELISA tests are a waste of time
and money if one considers that a positive alone is taken as of no value
alone, and a negative test makes little scientific, practical, or ethical
sense when used to exclude patients.
Not many have done acridine orange stains on buffy coat samples of
white blood cell concentrates but it looks easy and rewarding from
Lida Mattman's work in Cell Wall Deficient Forms- Stealth Pathogens Third
edition CRC Press 2000.
PCR testing of tissue samples
is more rewarding in sensitivity that fluid samples such as blood.
I think the likelihood of a positive blood PCR is probably about 15-20%
on first testing of a patient with Bb. This might indicate a need for serial
PCR DNA out to 6 or 7 samples before offering the patient much in the way
of confidence that Bb was unlikely to be present.
If you find the site discussing a full work up of the cns microbes please
share it.
Harold
Diagnostic Labs in Germany (von J.
Gr mailto:Joachim.Gruber@acamedia.info
uber):
Of related interest (added by J.
Gruber):
-
Testing for Neurotoxins
- Visual Contrast Sensitivity Test (VCS) in Chronic
Lyme
The VCS Exam demonstrates the effect of neurotoxins on
the optic nerve and the array of connected nerves in the cortex of the
brain. Additionally, we can use VCS Exam to monitor improvement with therapy.
Date: 10.4.2001
Address of this page is http://www.Lymenet.de/workup.htm
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