Re: a few things

a_weisman_at_yahoo.com
Date: 02/19/05 

Date: 19 Feb 2005 14:44:41 -0800

eugeneshapiroisapig wrote:

Let me begin by saying that I appreciate your obviously thoughtful
response.

> Well as far as steere's article goes...whether or not the guy had LD
is
> beside the point.
> These are just a few points:
> (1) Steere states that "currently neither...nor spect scan of the
brain
> have sufficient specificity to be helpful in diagnosis"
> Oh, so SPECT scanning isn't helpful, huh? That's slightly
> different wording from a paper Steere coauthored in Dec. 1997
Neurology
> "Therefore, quantitative SPECT provides an objective measurement of
the
> severity of the cerbral hypoperfusion in lyme encephelopathy and may
be
> used to help monitor response to therapy, but cannot be used ALONE to
> diagnose the condition."
> So basically in one paper he's saying it's not useful, in the
> other he's saying it is useful but shouldn't be used alone. Which is
> it? Obviously SPECT scanning doesn't tell you what is causing the
> hypoperfusion, but neither does taking a temperature tell you the
cause
> of a fever. the bottom line is it's obviously a useful adjutant to
the
> diagnostic algorithm, but steere has trouble admitting this for some
> reason.
> Steere, being a rheumatologist, should probably not worry
himself
> about diagnostic issues related to CNS infection. I honestly believe
he
> wants to "own" this disease and the only way that happens is if it is
> primarily rheumatological condition.

I think your points above are generally well made.

I do think it is quite fair to say, and Dr Fallon says himself in his
own articles, that SPECT scanning is NOT in and of itself diagnostic of
Lyme. It produces a pattern that is consistent with Lyme; but also
consistent with several other conditions.

So the SPECT results can do several things.

They can demonstrate objectively evidence of an organic process at work
(rather than hypochondria).

They can demonstrate a pattern CONSISTENT with (But not itself
diagnostic of) Lyme disease (though I personally would like to see some
more work helping to distinguish Lyme patients and those with and
without coinfections, assuming the patterns are different);

They can be used in conjunction with other test results, history, and
differential testing (used to exclude other conditions) to support a
diagnosis of Lyme;

They MAY be helpful in demonstrating the efficacy of treatment.

> 2. In discussing chronic lyme disease in the august 2002 article,
> steere mentions a study involving patients with a history of lyme
> disease who reported persistent symptoms after an initial round of
abx
> therapy and were treated with additional abx therapy. He states:
> "baseline assessments documented severe impairments in the patient's
> health-related quality of life. HOWEVER, ALL BASELINE CULTURES OF CSF
> IN BSK MEDIUM OR IN HYPOTONIC SALINE, A METHOD TO DETECT SPHEROPLAST
> L-FORMS, WERE NEGATIVE FOR BB. IN ADDITION, BB DNA WAS NOT DETECTED
BY
> PCR IN ANY BASELINE SAMPLES OF CSF...."
> This information is apparently presented as intending to support
> the idea that the patients who reported persistent symptoms could not
> have had active infection. In any event, the statement above is
> completely illogical and should not have appeared in the article. It
is
> horribly misleading as steere well knows. But don't take it from
> me...take it from Steere himself, for earlier in this same article he
> states"neither culture nor PCR testing has been of much value in
> patients with chronic neuroborreliosis. Bb has not been cultured from
> the CSF of such patients, and Bb DNA has been detected in only a
small
> number of them"
> OK, allen, which is it: Does this sort of testing have value, or
> doesn't it? Because if it doesn't have much value in
neuroborreliosis,
> then what's the point presenting the test results from the unknown
> chronically ill? Essentially, you've said it is useless. So if it is
> useless, how do you know these people don't have chronic
> neuroborreliosis?

I think you make some good points above. However, I am a bit troubled
when Lyme patients take the position (not saying you are) and use the
phrase "absence of proof is not proof of absence." The reason I find
this troubling is that the absence of proof is not the presence of
proof either.

One has to take into account the meaning of an absence of proof. And I
think your points above do that. So, for example, if one knows that
testing of spinal fluid is not particularly sensitive (it results in a
high number of false negatives based on controlled studies of patients
who definitely have CNS Lyme) then a negative result has less value.

It is troubling for patients (and doctors, meaning too many LLMDS) to
insist that it is Lyme no matter what!

I do firmly believe that the testing is quite unreliable and that it
results in too many false negatives, no matter what the source (blood,
CSF, joint fluid, skin biopsy of rash sites, etc.), and more so
depending on other factors too (timing of the test, prior treatment
etc.).

And I believe firmly that the diagnosis of Lyme, properly made is a
clinical one. That if one does as Liegner does for example, a lot of
differential testing to eliminate other possible explanations of a
patient's symptoms, and based on history, examination and the exclusion
of other possibilities, that this is a good basis for a clinical
diagnosis. I also think that one needs to keep in mind that ALL
diagnoses of ALL disease is provisional--basically it is a working
hypothesis. The diagnosis can be supported by observation of treatment
response (a patient has "herxes" and/or improves) (*caveat: I think
that what is, and what is not, a "herx" needs to be carefully
considered--the term "herx" is, in my opinion, overused, and is so
imprecise in many situations as to lose meaning).

I'd note, in this vein, that SPECT scanning which is NOT diagnostic
because it the pattern is NOT UNIQUE to Lyme, can be more useful if one
eliminate the other known disease entities which produce a similar
pattern. So if Lyme and three other things cause a similar pattern, one
can reliably eliminate the three other things, then the diagnosis of
Lyme is better supported. Usually this is a good idea in that testing
to rule in and rule out things other than Lyme tends to be MUCH more
reliable than lyme testing. This is true of other things on a
differential list for Lyme diagnosis too (so what produces fatigue and
flu like symptoms and fever and headaches etc--rule those things out
and Lyme becomes more and more likely).

So I support clinical diagnosis and empiric treatment. And treatment
based on symptom response rather than a cookbook approach--so instead
of three weeks is enough, let' see how a patient responds and base
treatment on that response.

> 3.steere includes a table in his article entitled "Lyme disease
> national surveillance case definition" He uses this data to make or
> exclude a diagnosis of lyme disease. However, the intent of the CDC
> algorithm is for reporting clear cases of LD for statistical
purposes,
> not for clinical diagnosis. As the CDC points out, but steere fails
to
> admit, LYME DISEASE IS A CLINICAL DIAGNOSIS. A PATIENT MAY HAVE LD
AND
> NOT FALL WITHIN THE SURVEILLANCE CASE DEFINITION. This is one of
> steere's worst little charades, and the one that causes the most
damage
> because it leaves GP's with an impression that the CDC criteria are
> strictly applicable. This method will necessarily exclude an unknown
> percentage of people from recieving the proper diagnosis. Which is
> basically the same thing as sentencing them to hell.

Yes VERY good point. The CDC surveillance criteria are clearly being
misused here.

Another point: without taking into consideration a patient's individual
history which may include travel to and/or recreation in, endemic or
hyperendemic areas, the use of these statistics is pointless.

Another point: What IF the patient is the first to have Lyme in their
area? If one were to automatically exclude Lyme based on no one having
had it previously in a given location, then no one will ever get
diagnosed.

This is also exactly contrary to the stated purpose of these (Very
faulty and underinclusive) statistics. One of the CDC stated
justifications for not using better epidemiologic techniques is that
the statistics are intended to gauge the spread geographically and the
overall increase of the disease. I don't agree that poor epidemiology
makes any sense and that is what it amounts to but that is amongst the
reasons they've stated and said that these are NOT intended for
diagnosis nor are they intended to give a true picture of the actual
incidence of the disease (in which case they'd use better epidemiologic
techniques and include categories for suspected Lyme, unconfirmed Lyme
etc.).

I do think that it is important to consider risk factors in an "index
of suspicion" and as FACTORS (not dispositive but factors to consider)
in whether it is more or less likely to be Lyme as part of a clinical
diagnosis. So factors such as geographic incidence, patient exposure,
risky activities (outdoor recreation in endemic areas) are things to
think about.

Of course, a patient can (easily) get Lyme with ONE exposure in their
own or someone else's backyard.

> 4. One more thing...I remember earlier steere was talking about emg
> test results in neuroborreliosis and he said something like "the
> patient did not have these tests."
> What the hell does that mean? Does it mean the tests weren't
performed,
> or that they were but the test results were negative? I think it
means
> the test wasn't performed. Now, I must ask why? Why weren't they
> performed?

Well I don't think a patient should be blamed for the fact that a
certain test wasn't performed and if Steere thought this was important,
why not make sure it was performed? It is basically citing a non factor
which should have no weight one way or the other. PLENTY of Lyme
patients have peripheral neuropathies without objective findings on
EMG; and peripheral neuropathies themselves wouldn't be diagnostic of
Lyme anyway (which I'm SURE that Allen would have pointed out IF there
were positive findings). Also, many Lyme patients may not have
peripheral neuropathies but do have Lyme.

So what did this add? Certainly nothing to add to the picture.

> there's more in this article, that's just what i remember from my
> notebook...more later. I'm exhausted. i just took a horrid four hour
> test on bacterial sugar transport systems and metabolic regulation
and
> crap like that.

Sounds fascinating! Get some rest. Thanks for the thoughtful comments.
I have some of my own to add, which I will add to the article itself.

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