Steere, 1991, Rheumatology News “Lyme Causes Everything”

From Kathleen Dickson:

Rheumatology News, April 1991 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 distruancesbut 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 havedistal 
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 sero-positive by ELISA, 
half of them had increased cerebrospinal 
fluid (CSF) protein,half had evidence of 
slight amounts of production of intrathecalantibody 
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 abnormal CSF anaysis, 
frequently accompanies by EMG evidence of 
an axonal neuropathy. 
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 Borrelia burgdorferi 
infection may cause a multiple sclerosis 
like picture [sic].

Dr Rudolf Ackermann in Cologne, Germany  
has described 44 such patients.  

So far we have seen only one: 6 years after 
disease 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 i

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 
Lymedisease.  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 sero-positive 
patients with late Lyme disease.
***I must emphasize the subtlety of the clinical 
picture in these sero-negative 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 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.***

About The Other Side Of The Stretcher

Nurse turned patient, but not by choice. I was became a Registered Nurse in 1985 when I was 21 years old. That career was cut short the end of 1994 when I was unable to work anymore because of the illness M.E. or Myalgic Encephalomyelitis. I have 3 adult children including twins, A daughter and 2 sons. View all posts by The Other Side Of The Stretcher

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