Autonomic dysfunction, small fiber neuropathy and Lyme disease

A new study published in PLoS ONE by Novak and colleagues suggests that small fiber neuropathy (SFN) may be a viable biomarker of post-treatment Lyme disease syndrome (PTLDS), particularly for patients whose main symptoms involve sensory issues.

 

The retrospective study included 10 patients diagnosed with post-treatment Lyme disease syndrome, who had autonomic testing performed between 2016 and 2018 at the Brigham and Women’s Faulkner Hospital Autonomic laboratory. [1]

The authors aimed to identify SFN as a possible biomarker of “PTLDS,” in addition to evaluating autonomic dysfunction associated with presumed small fiber neuropathy and assessing cerebral blood flow, since cognitive complaints may be due to cerebral hypoperfusion.

Novak and colleagues defined “PTLDS” using the Aucott’s criteria, which states that patients must have:

  1. A combination of fatigue, cognitive complaints and chronic widespread pain following the treatment of Lyme disease for at least a 6-months period;
  2. An absence of other disorders that can explain the complaints associated with “PTLDS”;
  3. A documented history of Lyme disease satisfying the CDC criteria.

Their 10 patients presented with a broad range of symptoms. The most common included lightheadedness (n=8), dry mouth or dry eyes (n=8), pale or blue feet (n=6), feet colder than the rest of the body (n=6), decreased sweating at feet at rest (n=5), and decreased sweating at feet after exercise or during hot weather (n=5).

post treatment lyme disease syndrome, chronic Lyme disease, chart, sensory disorder, autonomic dysfunction

Symptoms reported by study participants. (Click on image to enlarge.)

Pain was frequently reported and described as: aching pain (n=10), numbness (n=8), prickling sensation (n=8), burning pain (8), lancinating pain (6), and allodynia (n=6). (Allodynia refers to central pain sensitization following a normally non-painful stimulation.)

Less common symptoms were: sweating increased at hands (n=3), nausea, vomiting, or bloating after meal (n=2), persistent diarrhea (n=4), leaking of urine (n=3), persistent constipation (n=2), and difficulty in erection (n=1).

All of the subjects had previously undergone routine autonomic testing. Novak and colleagues performed skin biopsies from the right calf using a 3-mm circular disposable punch tool.

They found that more than 50% (7 out of 10) of patients had a low cerebral blood flow velocity (CBFv) from their middle cerebral artery. This was determined using a Transcranial Doppler. The study was not designed to determine if the low CBFv contributed to the cognitive impairment in those 7 patients.

All of the patients had a loss of small fibers, along with autonomic dysfunction and abnormal cerebral blood flow.

Sensory symptoms and pain reported by some patients with ongoing Lyme disease symptoms may be caused by small fiber neuropathy and a low cerebral blood volume, according to the authors of a new study. Click To Tweet

According to Novak, the sensory symptoms and pain reported by their patients may have been caused by small fiber neuropathy and low cerebral blood volume. “SFN appears to be associated with ‘PTLDS’ and may be responsible for certain sensory symptoms,” the authors write. “Dysautonomia related to SFN and abnormal CBFv also seem to be linked to ‘PTLDS’.”

Therefore, “Our study indicates that SFN may be an objective marker of ‘PTLDS’, at least in patients with prominent sensory symptoms,” Novak writes.

The study was not designed to address treatment. The authors assumed the patients did not have a persistent infection.

Editor’s note: I have been reluctant to use the term “PTLDS” until there is a reliable test to rule out a persistent infection.

References:
  1. Novak P, Felsenstein D, Mao C, Octavien NR, Zubcevik N (2019) Association of small fiber neuropathy and post treatment Lyme disease syndrome. PLoS ONE 14(2): e0212222. https://doi.org/10.1371/journal.pone.0212222
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8 Replies to "Autonomic dysfunction, small fiber neuropathy and Lyme disease"

  • Nancy Allen
    02/13/2020 (3:02 pm)
    Reply

    Dr. Cameron ,
    Have you observed erratic blood pressure, with orthostatic hypertension, in your Lyme patients ? If so, has antibiotic treatment resolved this complex issue ?

  • Petra
    01/25/2020 (8:42 pm)
    Reply

    Marker? you gotta be kidding me. What about systemic autoimmune diseases like Sjogren’s that cause SFN (and evven POTS) in youth without sicca and without positive antibodies,…how can SFN be a marker for Lyme.

    • Dr. Daniel Cameron
      01/26/2020 (1:18 pm)
      Reply

      That is the problem with any biomarker. Small fiber neuropathy can be seen in Lyme disease but may reflect the effects on the immune system. Other illnesses also affect the immune system. POTS is seen in Lyme disease through its effect on the autonomic nervous system. POTS can also have more than one cause.

      • Petra
        02/05/2020 (6:03 am)
        Reply

        Then I guess I have the definition of ‘marker’ wrong. I thought it means you have that specific disease.

        • Dr. Daniel Cameron
          02/05/2020 (10:14 am)
          Reply

          Biomarkers offer clues for the disease or how active the disease is. They are often not diagnostic on their own.

          • Petra
            02/06/2020 (6:33 am)

            I have for as long as I remember some kind of PANS, and dysautonomia (heat sensations in my feet, soon neuropathies), then from puberty prob POTS, Hashimoto too. My Lyme diagnosis was clinical, based on high positive Elispot/LTT, but only p83 on Western blot. I never had antibiotics for 20+ years of being symptomatic. Until 5 years ago when I had massive herx from just doxy, azithromycin, monotherapy. The herxing following 2 years made POTS worse and my ANA turned positive, with weak positive SSA. My POTS antibodoies (adrenergic and muscarinic receptors) were record high /700% increased../. I have family history of Sjogrens. Even though antibiotics got rid of many sympotms (facial neuropathy, some neuropsychiatric), seems like they further enhanced autoimmune component and in the end I got even Sjogren’s with classical sicca part. …… What baffles me is that research on Sjogren’s antibodies (early Sjo ) says 41% of POTS patients who have dryness but negative ANA/sjogrens (mind you, I was in the group without dryness!!!) has early Sjo antibodies,, so almost half patient with POTS if you count in those with official Sjogrens/lupus. At the same time I hear ILADS doctors saying that 50% of Lyme patients have POTS. Seems like neuro-Sjogrens, without sicca, often present in youth, is almost undistiguishable from Lyme. Another interesting thing that nobody speaks about is if 50% of Lyme patients have POTS, and 90% of POTS patients have alpha1 adrenergic (and some muscarinic) antibodies, would that mean there is strong connection of Lyme with adrenergic antibodies. As they recently published 1st appear Adrenergic in POTS, and later patients get muscarinic too (Sjogrens), and seems like that is how it was in me, 20 years of POTS and only then Sjogren’s. Dr Cameron, how often you see ANA test or even specific antibodies for lupus or Sjogrens, go negative from Lyme treatment? I am unsure if i should continue in that direction because I think antibiotics wreaked my gut, 2 years ago Rocephine caused severe damage to gut and then to brain too, and I got more neuroinflammation, still recovering 2 yrs later, I think it was leaky gut.

          • Dr. Daniel Cameron
            02/06/2020 (9:01 am)

            POTS is common in Lyme disease. I am sure the percentage. Rheumatologic diseases and Lyme disease overlap, in part, because they are both driven by an overactive immune status. We are only scratching the surface on what happens to the immune system during a tick-borne infection.

  • Gretchen
    03/09/2019 (3:15 pm)
    Reply

    Lyme is real! We need treatments that work. We need people to take us seriously.


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