Steere, 1991, Rheumatology News
Kathleen
Guest Commentary
Rheumatology Research in the 90s
By Allen C. Steere
Syphilis now has a competitor for the title of most complex infection.
Because of the neurologic
abnormalities it produces, Lyme disease is reminiscent of neurosyphilis.
***Once present, the neurologic symptoms follow a slowly progressive
course, in some instances for 10 years or longer.*** Most of these
patients have subtle encephalopathy affecting the central nervous
system. They have memory difficulty, depression, or sleep distruances
but no seizures, myoclonus, or changes in the level of consciousness.
They also have sensory symptoms, such as pain in the spine,
accompanied by radicular pain in the limbs or trunk, and some have
distal parethesias with intermittant tingling sensations in the hands
and feet.
These symptoms are perilously close to those that occur in fibromyalgia,
with the chronic fatigue syndrome, or instress-induced syndromes-
conditions that are ever so much more common than tertiary Lyme
disease. How then does one identify the patient with chronic neurologic
abnormalities of Lyme disease?
The patients in question have characteristic findings on laboratory
evaluations as follows:
almost all were seropositive by ELISA, half of them had increased
cerebrospinal fluid (CSF) protein,
half had evidence of slight amounts of production of intrathecal
antibody to the spirochete, and 70%
had one or more of both abnormalities. In addition, more than 50% had
abnormal EMGs indicating polyneuropathy affecting both proximal and
distal nerve segments, and MRI brain scans showing areas of increased T2
signal intensity.
In other words, many of our patients had memory impairments on their
psychological assessments, had adnormal CSF anaysis, frequently
accompanies by EMG evidence of an axonal neuropathy. A number of them
also had intermittant attacks of arthritis. Combined with the evidence
of immunity to Borrelia burgdorferi, this is the clinical picture that
is most suggestive of Lyme disease.
There is some provocative information that now suggests that B
burgdorferi infection may cause a multiple sclerosislike picture [sic].
Dr Rudolf Ackermann in Cologne, Germany has described 44 such
patients. So far we have seen only one: 6 years after diseae onset, the
patient experienced progressive stiffness and weakness in the muscles of
his right arm and in both legs; tendon jerks were diffusely brisk, with
bilateral ankle clonus and Babinski sign; and there were occasional
episodes of incontinence.
MRI of the brain revealed numerous small areas of increased T2 signal
intensity in the periventricular region on the right side. This scan is
compatible with the diagnosis of multiple sclerosis; however, in the
case of this patient, brain stem and auditory-evoked potentials were
normal, and he did not have myelin basic protein in CSF. What *did*
suggest Lyme disease was the fact that he had a serum IgG antibody
response to B burgdorferi of 1 to 12,800 and he had evidence of
intrathecal antibody production to the spirochete.
I want to emphasize that it is not yet proved that B burgdorferi causes
this syndrome. The patient could have two diseases- Lyme disease and
multiple sclerosis. What we lack is the discovery of the spirochete
from the brain lesions or the CSF, or perhaps proof of its presence by
polymerase chain reaction (PCR) amplification of borrelial gene
segments- a technique that is not quite perfected for use in Lyme
disease.
***If B. burgdorferi does cause this syndrome, it's absolutely amazing
that this spirochete would mimic not only rheumatoid arthritis (RA) but
also multiple sclerosis (MS), two of the most puzzling and devastating
autoimmune diseases.***
***Now I would like to proceed to the issue of seronegative Lyme
disease. I am convinced this entity exists.*** We have evaluated
approximately 200 patients with late Lyme disease in the past 2 years,
and we found that nine, or 5%, were seronegative by ELISA. This finding
coincides with the figure from Ray Dattwyler, MD, at Stony Brook (SUNY),
who first described seronegative Lyme disease. He stressed that this
outcome is more likely to occur in patients who receive antibiotic
therapy during the first several weeks of infection. Indeed, six of our
nine patients (67%) did receive antibiotic therapy during the first
month of illness, a significantly higher percentage than in our
seropositive patients with late Lyme disease.
***I must emphasize the subtlety of the clinical picture in these
seronegative patients. Two had erythema migrans followed months later by
very mild episodes of arthritis lasting only days. Three of the
patients had a subtle encephalopathy/polyneuropathy picture, resulting
in some memory disturbance accompanies by slight numbness and tingling
in the extremities. They also have CSF and EMG abnormalities. **Two of
the patients with neck pain had EMGs that revealed cervical
radiculopathy.** The two final patients had a more generalized pain
syndrome with tender points on examination- the clinical picture of
fibromyalgia. Three of the patients (one with arthritis and two with
neurologic abnormalities) had only a cellular immune response to the
spirochete.***
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Frank de Groot
It seems that in absense of a massive amount of data that proves 'our'
point,
the medical establishment is unable to use logic instead to interpret the
small amount of data.
Did Steere write this? Has he seen the light finally? Can I put him off my
death list? (just joking)
Frank
"Kathleen" <kathleen...@snet.net> wrote in message
news:f46dbd96.02050...@posting.google.com...
JMarie
12,2001 issue of NEJM - Medical Progress-Lyme Disease: We now know
that it is not the great imitator we once thought it was and sometimes
symptoms resolve without treatment. Fetal transmission rarely occurs
IF AT ALL.........ETC. ETC.
"Frank de Groot" <fran...@online.no> wrote in message news:<xaiA8.9765$ph2.2...@news4.ulv.nextra.no>...
Frank de Groot
He has been bought, like Microsoft buys competitors.
Frank de Groot
"JMarie" <marij...@aol.com> wrote in message
news:1c22167c.0205...@posting.google.com...