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When ALS Is Lyme” Amyotrophic Lateral Sclerosis, 2012; 13: 487–491 REVIEW ARTICLE ALS Untangled No. 17: “ When ALS Is Lyme ” The ALSUntangled Group The fi rst ALSUntangled, published in 2009, reviewed general) cognitive defi cits such as verbal fl uency (4). the possibility of a link between ALS and Lyme dis- Whether or not Lyme can cause brain damage in ease (1). We found no evidence for an increased fre- these same regions is controversial; if so, it is exceed- quency of positive Lyme tests in our cohort of 4000 ingly rare (5). Even if there is overlap in the brain patients with confi rmed diagnoses of ALS. We found regions affected by ALS and Lyme, a very general no evidence that any of the patients in our cohort coincidence/overlap between two conditions such as with a positive Lyme test had their ALS cured by this does not mean that they are causally related. The appropriate treatment for Lyme disease. Nonethe- Vaughters fail to mention that 90% of patients with less, rumours of a connection have persisted and a Lyme report or have a specifi c type of rash called number of “ Lyme literate ” clinics continue to adver- erythema migrans (6); PALS rarely, if ever, do. The tise their controversial testing and treatments for most common symptoms and signs of nervous sys- patients with ALS (PALS). One source of these per- tem Lyme disease are headache, stiff neck, photo- sistent rumours appears to be an online manuscript sensitivity and fever (from lymphocytic meningitis), called “ When ALS Is Lyme ” written by Sarah and reversible facial nerve palsy, eye movement abnor- John Vaughter (2) and available on their marketing malities, and mono- or oligo-radiculopathy that pro- website (3). Here, on behalf of PALS who requested duces dermatomal pain and sensory loss in addition it, we review this manuscript. to weakness (5). PALS do not present with head- For personal use only. ache, stiff neck, photosensitivity, fever or reversible facial weakness, and rarely have eye movement Arguments made for a connection between abnormalities, dermatomal pain or sensory loss. Lyme and ALS Thus, in reality, there is little overlap between the The Vaughters attempt to demonstrate that “ Lyme typical clinical picture of ALS and that of nervous is a frequent cause of ALS ” using the following argu- system Lyme disease. Very rarely, Lyme has been ments: a similarity of symptoms and anatomic abnor- reported to cause encephalomyelitis and/or polyra- malities in chronic Lyme and ALS, an overlap diculopathy. If these occurred together they could between the geographic and occupational distribu- produce upper and lower motor neuron signs (the tions of Lyme and that of ALS, an increased fre- hallmark of ALS), but again they should be accom- quency of positive serologic testing for Lyme in panied by clinical and laboratory features that are PALS, and cases of ALS and Lyme in which the not part of ALS such as pain, sensory loss, and focal former was said to improve with treatment of the infl ammatory changes on neuroimaging and/or spi- Amyotroph Lateral Scler Downloaded from informahealthcare.com by Bireme - Pauls Medical Library on 01/24/13 latter. We will now review each of these arguments. nal fl uid (5,7). First, the Vaughters state that PALS have general- Secondly, the Vaughters argue that geographic ized brain damage including cognitive changes, and locations and occupations with a high incidence of that those patients with Lyme disease also have gen- Lyme disease diagnosed by Centers for Disease eralized brain damage and cognitive changes. They Control (CDC) criteria also have a high incidence go on to conclude from this “ therefore most ALS of ALS. Again, here we see coincidence being patients have classical symptoms of neuroborrelio- accepted as causality. The authors downplay other sis ” . This is one of many examples of fl awed logic potential explanations for geographic and occupa- that appear in the manuscript. Post mortem and tional clusters of ALS (8). Furthermore, they again neuroimaging studies show that ALS targets specifi c fail to mention information that contradicts their motor and non-motor brain regions; involvement of hypothesis (including information in some of the frontal and temporal regions leads to specifi c (not very references they cite): the incidence of Lyme ISSN 1748-2968 print/ISSN 1471-180X online © 2012 Informa Healthcare DOI: 10.3109/17482968.2012.717796 488 The ALSUntangled Group disease in Italy is almost 30 times higher than in tests (6,14,16,17), this post cannot be considered Ireland (9), yet ALS incidence in these countries is useful scientifi c evidence. Next is a group of 414 similar (10); Hawaii had no Lyme reported between described by Qureshi (19). Here the testing for Lyme 2000 and 2010 (11) yet certainly has had patients included the above described Elisa and Western diagnosed with ALS; Guam, which historically has blots. The diagnosis of ALS was made at one of the had one of the highest incidences of ALS in the USA ’ s best hospitals (MGH). The Vaughters report world (12) has a very low incidence of Lyme (13). “ this study found 5.8% of ALS patients positive for Thirdly, the Vaughters argue that there is an Lyme, which is 67 times higher ” than the back- increased frequency of positive Lyme tests in patients ground population. They are referring to the fre- with ALS. In order to review this it is necessary to quency of positive Lyme Elisa tests (not those defi ne what is meant by a “ positive Lyme test ” . An confi rmed by Western blot) and they are comparing abundance of evidence suggests that Lyme testing of this to the background frequency of Lyme defi ned any variety should only be performed when there is by CDC criteria for the entire United States (with- a high clinical suspicion because false positives are out regard for the marked regional variation in so common (5,6,14). In our opinion this means that Lyme). In actuality, the study found four out of 414 PALS who do not have typical Lyme features such PALS to be positive for Lyme by the two-step method as rash, headache, stiff neck, photosensitivity, fever, (0.97%) and this is similar to the background rate reversible facial weakness, eye movement abnormal- of positive Lyme tests in the north-eastern United ities, dermatomal pain or sensory loss should not be States where these patients came from (19). Next tested at all. For patients with a clinical suspicion for they report on a study by Halperin (20). The Vaugh- Lyme disease, credible experts such as the Centers ters interpret this paper as showing “ 21 out of for Disease Control (15) agree that testing should 24 ALS patients that tested Lyme-positive, making start with an Elisa (enzyme linked immunoabsorbent it 88%, or almost nine out of ten patients ” . They go assay) and if that test is positive or equivocal then a on to say “ since the false negative rate of the tests Western immunoblot should be performed. There used is notoriously high, we are justifi ed in conclud- are very specifi c bands that defi ne a positive Western ing that, most likely, every single ALS patient in their blot (6,14). In the appropriate clinical setting, if both study was Lyme-positive ” . This interpretation is tests are positive, a patient can be considered “ posi- inaccurate for multiple reasons. We have already tive for Lyme ” . With this highly reliable (16) discussed that the false negative rate of the CDC approach, false negatives (concluding that a patient recommended Lyme testing is very small. Halperin does not have Lyme when they actually do) are van- performed a variety of Lyme tests on 56 (not 24) For personal use only. ishingly rare unless a patient is in the fi rst month of patients with motor neuron disease. While some had their illness (6,14); in these cases testing can be classic ALS (upper and lower motor neuron signs), repeated. In CNS Lyme there will be abnormalities others had other motor neuron diseases that would in the spinal fl uid including elevated white blood cell not meet accepted criteria for ALS (patients with counts and protein (5,7,14). The Vaughters claim pure lower motor neuron signs or pure upper motor that this approach is “ unreliable, ” that the Elisa has neuron signs) or had atypical features for ALS such “ up to 95% false negatives (depending upon which as sensory loss. Unfortunately, the tables in the expert you ask) ” and that the Western blot has “ up Halperin paper that list clinical characteristics do not to 60% false negatives ” . No references are given to include all 56 patients so it is not possible to clearly support these statements. They argue for a urine determine how many had classical ALS versus assay for Lyme, which clearly has been shown to be another motor neuron disease. However, the paper unreliable in peer reviewed literature (16). They does show that, in one very small sample from an claim that there is “ no such thing as a false positive” area with a high background rate of Lyme disease, a Amyotroph Lateral Scler Downloaded from informahealthcare.com by Bireme - Pauls Medical Library on 01/24/13 Lyme test; this statement contradicts multiple larger percentage of patients with motor neuron published reports (6,14,16,17). disease tested positive for Lyme (9/19 or 47%) com- Against this background the Vaughters review the pared to patients without motor neuron disease results of Lyme testing in various groups of patients (4/38 or 11%). Halperin correctly concludes in this reported to have ALS.
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