Bannwarth Syndrome: An Unusual Neurologic Manifestation of Lyme Disease
Bannwarth syndrome is a neurologic form of Lyme disease.
It can cause painful radiculopathy, neuropathy, and facial palsy.
Although more common in Europe, U.S. cases are increasingly recognized.
Bannwarth syndrome, also known as Garin-Bujadoux-Bannwarth syndrome, is a manifestation of Lyme neuroborreliosis characterized by painful radiculopathy, peripheral neuropathy, varying degrees of motor weakness, facial nerve palsy, and cerebrospinal fluid lymphocytic pleocytosis. Although it has traditionally been reported more frequently in Europe, an increasing number of cases have been reported in the United States.
In 2018, physicians at Mayo Clinic described five patients with Bannwarth syndrome from Minnesota and Wisconsin, highlighting that this neurologic manifestation also occurs in North America. Their patients presented primarily with painful radiculopathy and peripheral neuropathy.
A 2019 case report by Diaz¹ describes a 60-year-old U.S. patient with a variant of Bannwarth syndrome highlighting that this neurologic manifestation of Lyme disease can occur in North America. The man initially presented with elevated liver function tests and an unintended weight loss of approximately 25 pounds.
For three weeks, he experienced progressive back pain along with peripheral neuropathy, including arm and leg weakness, numbness in his hands, and a right facial droop. Shortly after admission to the hospital, he developed complete facial palsy.
“Throughout this time, severe central back pain persisted requiring neuropathic pain agents and opiates for adequate pain control,” Diaz wrote.
An electromyography (EMG) and nerve conduction study demonstrated prolonged distal latencies and slowed conduction velocities consistent with polyradiculopathy.
Cerebrospinal fluid analysis revealed lymphocytic pleocytosis (96%) and elevated protein (156 mg/dL), findings supportive of Lyme neuroborreliosis in the appropriate clinical setting.
Serum and cerebrospinal fluid testing were positive for Lyme disease by IgG Western blot. Serum testing revealed only one IgM band. A cerebrospinal fluid-to-serum antibody index was not performed.
Anaplasmosis was considered as the cause of the elevated liver enzymes, but testing was negative. Serologic testing was positive for Babesia exposure, although no parasites were identified on blood smear.
The patient’s evaluation led to a diagnosis of a variant of Bannwarth syndrome, and he was treated successfully with four weeks of intravenous ceftriaxone.
At a two-month follow-up, his facial paralysis, pain, motor deficits, and sensory abnormalities had resolved, and both his weight and liver function tests had returned to baseline.
“Our case demonstrates the importance of consideration of Bannwarth syndrome in the differential diagnosis of meningoradiculitis, even in the setting of atypical features such as liver dysfunction and weight loss,” Diaz wrote.
Frequently Asked Questions
What is Bannwarth syndrome?
Bannwarth syndrome is a neurologic manifestation of Lyme disease characterized by severe painful radiculopathy, peripheral neuropathy, motor weakness, facial nerve palsy, and cerebrospinal fluid lymphocytic pleocytosis.
Is Bannwarth syndrome seen in the United States?
Although historically reported more commonly in Europe, published case series and case reports demonstrate that Bannwarth syndrome also occurs in the United States and may be underrecognized.
How is Bannwarth syndrome treated?
Treatment generally consists of appropriate antibiotic therapy for Lyme neuroborreliosis. In this case, the patient recovered following four weeks of intravenous ceftriaxone.
Clinical Takeaway
Although Bannwarth syndrome has traditionally been associated with Europe, published U.S. case reports and case series indicate that clinicians should also recognize this syndrome in North American patients.
Severe radicular pain accompanied by peripheral neuropathy, facial palsy, or motor weakness should prompt consideration of Lyme neuroborreliosis, particularly in endemic regions. Early recognition and appropriate antibiotic treatment can lead to substantial neurologic recovery, even in patients with atypical accompanying features such as weight loss and elevated liver enzymes.
Related Articles
Learn more about neurologic manifestations of Lyme disease:
Six cases of neuroinvasive Lyme disease
Neurologic Lyme disease: symptoms and diagnosis
Femoral neuropathy as a neurologic symptom of Lyme disease
Lyme disease symptoms guide
References
- Diaz MM, Wesley SF. Meningoradiculitis and transaminitis from neuroborreliosis: A case of variant Bannwarth syndrome. Clin Neurol Neurosurg. 2019;186:105532.
- Omotosho YB, Sherchan R, Ying GW, Shayuk M. A Unique Case of Bannwarth Syndrome in Early Disseminated Lyme Disease. Cureus. 2021;13(4):e14680.
- Shah A, O’Horo JC, Wilson JW, Granger D, Theel ES. An Unusual Cluster of Neuroinvasive Lyme Disease Cases Presenting With Bannwarth Syndrome in the Midwest United States. Open Forum Infect Dis. 2018;5(1):ofx276.
Dr. Daniel Cameron, MD, MPH
Lyme disease clinician with over 30 years of experience and past president of ILADS.
Symptoms • Testing • Coinfections • Recovery • Pediatric • Prevention
Dr Cameron,
have you ever seen a case of Kluver Bucy from Lyme or any of the coinfections? Hyperphagia and visual agnosia as dominant. I am confident KBS describes the condition because I got prosopagnosia from antibiotics. Many symptoms vary in intensity but it’s never as before onset of POTS/Hashimoto/SFN
there was nothing on MRI and spinal tap was normal.
Although both were done 15 years after the onset.
The symptoms started along with Hashimoto, POTS, and numbness of the left face.15 years later I found out I also have Sjogrens which was presenting as POTS but now also sicca (15+ yrs no sicca but only mild parotid swelling from start of disease)
I read KBS might come from tirgeminal nerve path virus entering the head?
-But I am negative to HSV1/2 even.
mycoplasma negative
chlamydia IgG pos,
Lyme LTT high positive, after it become negative not much help in KBS
my KBS symptoms do respond to essential oils antibiotics and to IVIG, but never fully. Overall 3+ years of various antibiotics just made me worse and tons of herxing but my autoimmunity grew stronger it seems.
I wonder if it’s gut related, there seems like low grade inflammation of my head but especially areas linked to KBS symptoms.
Thank you
Kluver Bucy syndrome is a rare behavioral impairment characterized by inappropriate sexual behaviors and mouthing of objects. Other signs and symptoms include a diminished ability to visually recognize objects, loss of normal fear and anger responses, memory loss, distractibility, seizures, and dementia according to https://rarediseases.info.nih.gov/diseases/6840/kluver-bucy-syndrome I have not seen KBS.
I was recently diagnosed with Bannwarth syndrome after suffering for nearly 3 years with nerve issues. Saw lots of doctors before finally a very posity test. (3 IGM, 8 IGG). I completed two rounds of doxy and 30 days of ceftriaxon IV.
After the neurologists, one said Bannwarth, who said your nerves are damaged and live with it. I’m already taking hydrocodone daily, with propanalol for tremors.
I’m having a real hard time accepting ” live with it”. Do you know if anything that can treat this horrible syndrome?
Dr. Cameron, I have a friend who started showing signs of lyme disease a year ago. I told her to get tested for it. Her provider refused and told her she didn’t need to be tested for it. After a year of her declining, they finally did a test. IGM positive Lyme total AB EIA positive. The provider proceeded to tell her that she does not have Lyme and was “only exposed to it”. She started having visual disturbances that she described as a rainbow. She went to a neurologist, they told her migraines. Started her on topamax. She started having severe swelling in her legs, so they put her on a thiazide to help pull the fluid off her legs and feet. She has continued to decline and is now on the verge of giving up. She went from 170 pounds to 95 pounds in a span of 6 months. Her PCP continues to tell her that there is nothing wrong with her. She eats and has been trying to gain weight. She stopped the topamax months ago bc she had lost so much, but continues to go down in weight. She now has neuropathy, sleeps all the time, she has a hard time walking and has to hold on to something or she can’t get around. If you have any suggestions, or would be willing to see her. I strongly believe that she has a coinfection present. The PCP’s that don’t understand Lyme disease or the risks that come with it. I have a very good friend who came to you, and that is why I am messaging you. Thank you so much for your time.
I am still seeing patients with similar presentations to your friend. I wish the tests were more reliable. You can direct your question to my office.