Lyme neuroborreliosis as described in 1999

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Spanky
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Re: Lyme neuroborreliosis as described in 1999

Post by Spanky » Fri 7 Sep 2012 17:31

"Carina":
Early Lyme (even if it a neuroborreliosis) is not a late (I talk about time) infection.
What they are saying that the distinctions that you INSIST on making OVER AND OVER AND OVER again... are not particualrly relevant.

Argue with them.

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Re: Lyme neuroborreliosis as described in 1999

Post by X-member » Fri 7 Sep 2012 17:33

I understand what THEY are saying, Spanky.

But do YOU understand it?

Edit to add:

Spanky, check WHERE you find the information that you post instead.

Then maybe YOU will understand WHAT THEY are talking about.

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Spanky
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Re: Lyme neuroborreliosis as described in 1999

Post by Spanky » Fri 7 Sep 2012 17:40

"Carina":
I understand what THEY are saying, Spanky.
I doubt that very much.

Why don't you tell us, then, what your understanding is of what is being said there?

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Re: Lyme neuroborreliosis as described in 1999

Post by X-member » Fri 7 Sep 2012 17:49

Spanky, I think it will be much more easy to understand the definition early and late Lyme disease (no matter where in the body it is located) without the quote from IDSA.

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Spanky
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Re: Lyme neuroborreliosis as described in 1999

Post by Spanky » Fri 7 Sep 2012 17:51

"Carina":
Spanky, I think it will be much more easy to understand the defintion early and late Lyme disease (no matter where in the body it is located) without the quote from IDSA.

:lol: Yeah, that's what I thought...

duncan
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Re: Lyme neuroborreliosis as described in 1999

Post by duncan » Fri 7 Sep 2012 18:01

Spanky, technically, the panel speculates here ("...differences may be related..."). So, maybe it would be fair to speculate that the distinction referenced can be attributed to both duration of infection, and "degree of involvement". Incidentally, I can interpret that last phrase in a number of ways.

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Spanky
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Re: Lyme neuroborreliosis as described in 1999

Post by Spanky » Fri 7 Sep 2012 18:10

"duncan":
Spanky, technically, the panel speculates here ("...differences may be related..."). So, maybe it would be fair to speculate that the distinction referenced can be attributed to both duration of infection, and "degree of involvement".
I don't see use of the word "may" as "speculation"...so much as advice to the physician not to discount the possibility that neuro symptoms may appear in someone who is "early stage" in terms of the progression of the illness. It seems fairly clear.

And that several studies show that there is no real sound basis for the rigid stage distinctions (as to neuro). Notice that there are citations for that statement.
Incidentally, I can interpret that last phrase in a number of ways.
Meaning?

duncan
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Re: Lyme neuroborreliosis as described in 1999

Post by duncan » Fri 7 Sep 2012 18:18

Meaning degree of involvement could involve several different metrics, or not. Ambiguity here favors the author, not the reader.

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Re: Lyme neuroborreliosis as described in 1999

Post by Spanky » Fri 7 Sep 2012 18:25

"duncan":
Meaning degree of involvement could involve several different metrics, or not. Ambiguity here favors the author, not the reader.
Meaning?

Once again, here is the quotation:
The panel has differentiated between early and late neurologic Lyme disease in these guidelines, as is customary. There is little evidence to support a pathophysiological basis for this distinction, however, and differences may be related more to the degree of involvement [208, 217, 219].
Now, using the customary and ordinary rules of grammar and sentence construction of the English language...

...what is it that the phrase: "There is little evidence to support a pathophysiological basis for this distinction"...refers to?

Clearly, it refers to the (distinction): "... between early and late neurologic Lyme disease in these guidelines, as is customary".

RitaA
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Re: Lyme neuroborreliosis as described in 1999

Post by RitaA » Fri 7 Sep 2012 21:08

Spanky wrote:"RitaA":
The name of the article doesn't really do it justice. It contains a lot of detailed information about the differences between early and late neuroborreliosis. The authors also describe differences between neuroborreliosis in Europe and North America.
Here is a section from the IDSA Guidelines. Notice that they are clearly saying that there is no real support for the early/late stage distinctions.

I have posted this many times, here...
The panel has differentiated between early and late neurologic Lyme disease in these guidelines, as is customary. There is little evidence to support a pathophysiological basis for this distinction, however, and differences may be related more to the degree of involvement [208, 217, 219].
http://cid.oxfordjournals.org/content/4 ... ull#sec-28

Posting out-dated material will often appear to cause some false sense, perception of contradiction, inconsistency.
Spanky,

The title of this thread clearly indicates that I was posting an article about how Lyme neuroborreliosis was viewed and described in 1999. Some of the published articles used to support the current IDSA guidelines are even older than this. Just for the record, I didn't notice any contradictions between the 1999 article and the IDSA guidelines, and there's no mention of the guidelines in my post.

Perhaps the IDSA guideline authors ought to consider updating the current guidelines to eliminate any arbitrary distinction between early and late neurologic Lyme disease if there truly is none. What I did notice in both the 1999 article and the IDSA guidelines (since you brought them up) is the fact that people diagnosed with late neurologic Lyme disease may respond more slowly and incompletely to treatment -- and this is one noteworthy difference (at least in my view).

http://cid.oxfordjournals.org/content/43/9/1089.full
Lyme meningitis and other manifestations of early neurologic Lyme disease. The use of ceftriaxone (2 g once per day intravenously for 14 days; range, 10–28 days) in early Lyme disease is recommended for adult patients with acute neurologic disease manifested by meningitis or radiculopathy (B-I). Parenteral therapy with cefotaxime (2 g intravenously every 8 h) or penicillin G (18–24 million U per day for patients with normal renal function, divided into doses given every 4 h), may be a satisfactory alternative (B-I). For patients who are intolerant of β-lactam antibiotics, increasing evidence indicates that doxycycline (200–400 mg per day in 2 divided doses orally for 10–28) days may be adequate (B-I). Doxycycline is well absorbed orally; thus, intravenous administration should only rarely be needed.

For children, ceftriaxone (50–75 mg/kg per day) in a single daily intravenous dose (maximum, 2 g) (B-I) is recommended. An alternative is cefotaxime (150–200 mg/kg per day) divided into 3 or 4 intravenous doses per day (maximum, 6 g per day) (B-II) or penicillin G (200,000–400,000 units/kg per day; maximum, 18–24 million U per day) divided into doses given intravenously every 4 h for those with normal renal function (B-I). Children ⩾8 years of age have also been successfully treated with oral doxycycline at a dosage of 4–8 mg/kg per day in 2 divided doses (maximum, 100–200 mg per dose) (B-II).

Although antibiotic treatment may not hasten the resolution of seventh cranial nerve palsy associated with B. burgdorferi infection, antibiotics should be given to prevent further sequelae (A-II). Cranial nerve palsies in patients with Lyme disease are often associated with a lymphocytic CSF pleocytosis, with or without symptoms of meningitis. Panel members differed in their approach to the neurologic evaluation of patients with Lyme disease–associated seventh cranial nerve palsy. Some perform a CSF examination on all such patients. Others do not because of the good clinical response with orally administered antibiotics (even in the presence of CSF pleocytosis) and the absence of evidence of recurrent CNS disease in these patients. There was agreement that lumbar puncture is indicated for those in whom there is strong clinical suspicion of CNS involvement (e.g., severe or prolonged headache or nuchal rigidity). Patients with normal CSF examination findings and those for whom CSF examination is deemed unnecessary because of lack of clinical signs of meningitis may be treated with a 14-day course (range, 14–21 days) of the same antibiotics used for patients with erythema migrans (see above) (B-III). Those with both clinical and laboratory evidence of CNS involvement should be treated with regimens effective for Lyme meningitis, as described above (B-III).

[snip]

Late neurologic Lyme disease. Adult patients with late neurologic disease affecting the central or peripheral nervous system should be treated with intravenous ceftriaxone for 2 to 4 weeks (B-II). Cefotaxime or penicillin G administered intravenously is an alternative (B-II). Response to treatment is usually slow and may be incomplete. Re-treatment is not recommended unless relapse is shown by reliable objective measures. Ceftriaxone is also recommended for children with late neurologic Lyme disease (B-II). Cefotaxime or penicillin G administered intravenously is an alternative (B-III). See the recommendations above on the treatment of Lyme meningitis for suggested doses of each of these antimicrobials.

[snip]

Background and Diagnosis of Early Neurologic Lyme Disease

Manifestations of acute peripheral nervous system involvement in Lyme disease include radiculopathy, cranial neuropathy, and mononeuropathy multiplex (multifocal involvement of anatomically unrelated nerves) [107–109, 111, 149–151]. CNS involvement includes lymphocytic meningitis and, rarely, encephalomyelitis (parenchymal inflammation of brain and/or spinal cord, with focal abnormalities evident on neurologic examination and imaging studies) [107–109, 111, 149–152]. Encephalomyelitis will be discussed in the section on late nervous system Lyme disease.

Although, in the 1980s, early neurologic Lyme disease was reported to occur in approximately 10%–15% of untreated patients with Lyme disease in the United States [107, 153, 154], the frequency of this manifestation is less in recent series [23, 26, 87–89], possibly because of bias of ascertainment in early studies or improved recognition and treatment of patients with erythema migrans. In the United States, cranial neuropathy is the most common manifestation of early neurologic Lyme disease [4]. Seventh nerve palsy is the most common of the cranial neuropathies, and bilateral involvement may occur [155, 156]. In areas where Lyme disease is endemic, ∼1 in 4 patients who present with seventh nerve palsy in nonwinter months can be shown to have Lyme disease [157]. Seventh nerve palsy due to Lyme disease can develop in patients who have no recollection of an erythema migrans lesion or of a tick bite.

[snip]

Background and Diagnosis of Late Neurologic Lyme Disease

Late neurologic Lyme disease may present as encephalomyelitis, peripheral neuropathy, or encephalopathy [/color][149–152, 208–212]. Because most patients with Lyme disease are now diagnosed and treated early in the course of infection, these more indolent forms of neurologic Lyme disease are quite rare. Encephalomyelitis is a unifocal or multifocal inflammatory CNS disease [152, 213]. Collectively, only 1 patient with encephalomyelitis has been diagnosed over the past 5 years by panel members (G.P.W., J.J.H., R.B.N., R.J.D., A.C.S., E.D.S., M.S.K., P.J.K., J.S.B., and L.B.), in spite of both community-based and referral clinical practices. This severe neurologic manifestation of Lyme disease has been diagnosed primarily in Europe.

In untreated patients, encephalomyelitis has been monophasic and slowly progressive, principally involving white matter. Two-tier (ELISA and IgG immunoblot) seropositivity with serum samples and evidence of intrathecal antibody production to B. burgdorferi are expected [149, 162, 213]. Intrathecal antibody production, however, may persist for years following successful treatment, so this parameter does not provide a useful marker of disease activity [214]. CSF examination typically shows a lymphocytic pleocytosis, a moderately elevated protein level, and a normal glucose level [149, 213]. Sensitivity of PCR for detection of B. burgdorferi DNA in the CSF of such patients is extremely low. MRI of the affected part of the neuraxis can demonstrate areas of inflammation, typically with increased signal on T2 and FLAIR imaging and enhancement following contrast administration [149, 215].

Lyme encephalomyelitis may be confused clinically with a first episode of relapsing-remitting multiple sclerosis or primary progressive multiple sclerosis, but appropriate CSF and serum studies for B. burgdorferi–specific antibody should differentiate between these entities in most instances [216–218].

Late neurologic Lyme disease–associated peripheral neuropathy typically presents as a mild, diffuse, “stocking glove” process. Only 9 such patients have been diagnosed by panel members (G.P.W., J.J.H., R.B.N., R.J.D., A.C.S., E.D.S., M.S.K., P.J.K., J.S.B., and L.B.) over the past 5 years. Patients typically complain of intermittent limb paresthesias, and some patients complain of radicular pain. The most frequent abnormality found on neurologic examination is reduced vibratory sensation of the distal lower extremities. Electrophysiologic studies show findings consistent with a mild confluent mononeuritis multiplex [219]. Nerve biopsy reveals small perivascular collections of lymphocytes, without spirochetes [220, 221]. Serum IgG antibody to B. burgdorferi detected by the 2-tier approach is expected in patients with Lyme disease–associated peripheral neuropathy. The absence of antibody should lead to an alternative diagnosis [149]. Because the pathophysiologic process usually occurs outside the subarachnoid space, CSF findings are often normal, without evidence of intrathecal antibody production to B. burgdorferi.

Lyme disease–associated encephalopathy is an imprecisely defined clinical entity characterized by mild abnormalities of memory and cognitive functions that are demonstrable either by a careful mental status examination or by formal neuropsychologic testing [211, 222]. Panel members (G.P.W., J.J.H., R.B.N., R.J.D., A.C.S., E.D.S., M.S.K., P.J.K., J.S.B., and L.B.) have diagnosed only 7 patients over the past 5 years. In the past, certain patients with this condition had concomitant Lyme arthritis [211]. In such patients, CSF examination findings were often normal, and the process may have been related to general illness rather than CNS infection (i.e., “toxic-metabolic” in origin). Other patients have had evidence of intrathecal antibody production to B. burgdorferi and/or increased CSF protein levels, with or without a mild CSF pleocytosis [208, 211, 222]. In these cases, the encephalopathy may actually be a mild form of encephalomyelitis. Cranial imaging studies may occasionally demonstrate focal areas of presumed parenchymal inflammation. Most often, findings are normal or demonstrate only minor, nonspecific abnormalities; consequently, cranial imaging plays little if any role in the diagnosis or follow-up of patients with this entity [223]. In serum, 2-tier IgG seropositivity is expected [149, 208, 211, 222, 223].

The panel has differentiated between early and late neurologic Lyme disease in these guidelines, as is customary. There is little evidence to support a pathophysiological basis for this distinction, however, and differences may be related more to the degree of involvement [208, 217, 219].
Perhaps the next update of the IDSA guidelines will blend the sections about early and late neurologic Lyme disease in order to eliminate some of the confusion that currently exists for doctors and patients alike.

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