Can Lyme Disease Mimic Guillain-Barré Syndrome?

Lyme neuroborreliosis can resemble Guillain-Barré syndrome
Weakness, facial palsy, and nerve findings may overlap
Two cases show why diagnosis can be difficult

Can Lyme disease mimic Guillain-Barré syndrome? Yes. Although uncommon, Lyme neuroborreliosis can produce weakness, numbness, reduced reflexes, facial palsy, radicular pain, and other neurological findings that resemble Guillain-Barré syndrome (GBS).

A 2026 case report provides a striking example. A 73-year-old man presenting in Texas developed severe back and radicular pain, leg weakness, reduced reflexes, and bilateral facial weakness. Clinicians initially considered an atypical form of Guillain-Barré syndrome and began intravenous immunoglobulin (IVIG). Further evaluation instead supported Lyme neuroborreliosis presenting as Bannwarth syndrome.¹

The patient had no known tick bite or erythema migrans rash. The possible source of exposure became apparent only after clinicians learned that he had traveled three months earlier to Pennsylvania, where he had spent time cutting and moving logs in the woods.¹

An earlier case looked even more like classic GBS. A 33-year-old man developed ascending weakness, numbness, bilateral facial palsy, reduced reflexes, and eventually respiratory failure. His spinal fluid and electrodiagnostic studies also supported a GBS-like demyelinating process, yet further testing ultimately supported Lyme neuroborreliosis.²

Together, these cases illustrate why neurologic Lyme disease may deserve consideration when patients develop an unusual GBS-like illness, particularly when facial palsy, radicular pain, possible tick exposure, travel to an endemic area, or other findings suggest Lyme neuroborreliosis.

What Is Guillain-Barré Syndrome?

Guillain-Barré syndrome is an immune-mediated neurological disorder affecting peripheral nerves. It can cause progressive weakness, numbness, tingling, loss of reflexes, and, in severe cases, paralysis affecting breathing.

GBS often develops after an infection. According to the National Institute of Neurological Disorders and Stroke, symptoms can range from mild weakness to severe paralysis, including an inability to breathe independently.³

The Cleveland Clinic notes that symptoms often begin within several weeks after an infection. GBS may also occur after surgery and, rarely, after vaccination.⁴

Lyme neuroborreliosis is different. It results from neurological involvement with Lyme borreliosis and may affect the meninges, cranial nerves, peripheral nerves, and nerve roots.

Because some of the resulting symptoms overlap with GBS, distinguishing the two conditions can sometimes be difficult.

2026 Case: Bannwarth Syndrome Mimicked Guillain-Barré Syndrome

Bhattarai and colleagues reported the case of a 73-year-old man who presented to a hospital in Texas with two weeks of back pain and generalized weakness, five days of left leg weakness, and two days of facial weakness.¹

His pain extended from the thoracic to lumbar region. He also experienced low back pain radiating into his left buttock and knee and thoracic pain radiating toward the left shoulder blade.

Before hospitalization, the back pain had been diagnosed as sciatica. Treatment with meloxicam, acetaminophen, gabapentin, and cyclobenzaprine did not adequately control the pain, which became particularly severe at night and interfered with sleep.¹

Neurological examination subsequently revealed several findings that could resemble Guillain-Barré syndrome:

• Bilateral facial weakness
• Left leg weakness
• Reduced knee reflexes
• Absent Achilles reflexes
• Abnormal sensory findings
• Severe radicular pain

Because of the combination of facial weakness, paresthesias, limb weakness, and reduced reflexes, clinicians initially considered an atypical Guillain-Barré syndrome variant.¹

The Spinal Fluid Pointed Away From Classic GBS

One of the most important clues came from the patient’s cerebrospinal fluid.

His CSF contained 226 white blood cells per microliter, predominantly lymphocytes, along with markedly elevated protein of 215 mg/dL.¹

This differed from the classic spinal fluid pattern often associated with Guillain-Barré syndrome. GBS commonly produces albuminocytologic dissociation—elevated CSF protein without a substantial increase in white blood cells.

In this patient, the significant lymphocytic pleocytosis instead supported an infectious or inflammatory meningoradiculitis.

This distinction became particularly important because the patient’s clinical symptoms alone could have suggested GBS.

MRI Showed Facial Nerve and Cauda Equina Involvement

MRI provided another important clue.

Brain imaging demonstrated enhancement involving segments of both facial nerves. Spinal MRI showed enhancement of the cauda equina nerve roots, consistent with inflammatory radiculitis.¹

The combination of severe radicular pain, bilateral facial palsy, CSF inflammation, and nerve-root enhancement raised concern for Lyme neuroborreliosis.

Interestingly, focused nerve conduction testing showed normal F-wave latencies. This contrasted with some of the electrodiagnostic abnormalities that may occur with classic Guillain-Barré syndrome.

He Did Not Recall a Tick Bite or Lyme Rash

The patient lived and presented in Texas, a state with relatively low reported Lyme disease incidence.

He also denied a known tick bite, erythema migrans rash, flu-like illness, joint symptoms, or other typical early Lyme disease manifestations.¹

Further questioning, however, uncovered an important exposure history.

Three months before becoming ill, he had traveled to Pennsylvania. During the trip, he spent time in wooded areas cutting and moving logs.¹

This case illustrates why a patient’s current location does not necessarily identify where a tick-borne infection was acquired. A careful travel and outdoor exposure history can be important when evaluating unexplained neurological illness.

Lyme Testing Supported Neuroborreliosis

Serum modified two-tier Lyme testing was positive, with both IgM and IgG antibodies detected. Lyme antibodies were also detected in the cerebrospinal fluid.¹

The authors considered the combination of findings clinically decisive:

• Severe radicular pain
• Bilateral facial palsy
• CSF lymphocytic pleocytosis
• Markedly elevated CSF protein
• Facial nerve enhancement
• Cauda equina nerve-root enhancement
• Positive serum and CSF Lyme antibody testing

Taken together, these findings supported Lyme neuroborreliosis presenting as Bannwarth syndrome rather than primary Guillain-Barré syndrome.¹

What Is Bannwarth Syndrome?

Bannwarth syndrome is a neurological manifestation of Lyme borreliosis characterized by painful meningoradiculitis.

Patients may develop severe radicular or nerve-root pain along with sensory abnormalities, weakness, and cranial neuropathies such as facial palsy.

Bannwarth syndrome is reported more frequently in Europe but can also occur in the United States. Because weakness and reduced reflexes may accompany the illness, the presentation can sometimes resemble Guillain-Barré syndrome.

The prominent pain can be an important clue. In the 2026 case, severe radicular pain combined with inflammatory CSF findings helped clinicians distinguish Lyme meningoradiculitis from classic GBS.¹

IVIG Was Started Before the Diagnosis Changed

Because clinicians initially suspected an atypical Guillain-Barré syndrome variant, IVIG was started empirically.

It was subsequently discontinued after the CSF findings and Lyme testing supported infectious meningoradiculitis rather than an immune-mediated polyradiculoneuropathy.¹

The patient was treated with doxycycline 100 mg twice daily for 28 days.

At two-month follow-up, his facial weakness had improved substantially, his left leg strength had returned to normal, his chest numbness had resolved, and his back pain had improved. No recurrent radicular pain or new neurological deficits were reported.¹

An Earlier Lyme Case Looked Even More Like Classic GBS

The distinction between Lyme neuroborreliosis and Guillain-Barré syndrome is not always straightforward. An earlier case reported by Farr and Bittar demonstrates just how closely the two conditions can overlap.²

A previously healthy 33-year-old man developed tingling and numbness in his hands and feet followed by progressive ascending weakness. Examination revealed bilateral facial palsy, reduced knee and ankle reflexes, sensory loss, and weakness affecting both legs.²

He did not recall a tick bite. However, he frequently played disc golf in wooded areas and reported a fever and blotchy abdominal rash shortly before his neurological symptoms began.²

Even the Spinal Fluid and Nerve Studies Looked Like GBS

The initial diagnostic findings strongly supported Guillain-Barré syndrome.

His cerebrospinal fluid contained no white blood cells but had mildly elevated protein, producing albuminocytologic dissociation—a classic finding associated with GBS.²

MRI of the lumbar spine showed enhancement of the cauda equina nerve roots. Electrodiagnostic testing demonstrated prolonged distal motor latency, conduction block, absent F-wave responses, and other findings interpreted as acute inflammatory demyelinating polyneuropathy.²

Based on the ascending weakness, reduced reflexes, spinal fluid findings, MRI abnormalities, and nerve conduction studies, clinicians treated him with a five-day course of IVIG for presumed Guillain-Barré syndrome.

His Neurological Illness Continued to Progress

Despite IVIG, the patient’s condition worsened dramatically.

His respiratory function declined, requiring intubation and eventually a tracheostomy. By hospital day eight, he had severe weakness involving all four extremities and loss of sensation throughout his arms and legs.²

Additional neurological abnormalities subsequently appeared, including abnormal eye alignment and bilateral ptosis. Brain MRI demonstrated enhancement involving multiple cranial nerves, including cranial nerves III, VII, and VIII, suggesting more widespread neurological inflammation.²

The continued deterioration despite treatment for presumed GBS, together with the preceding rash, outdoor exposure, bilateral facial palsy, and evolving cranial neuropathies, prompted clinicians to investigate Lyme disease.

Lyme Testing Changed the Diagnosis

Lyme antibodies were detected in both serum and cerebrospinal fluid. The initial Western blot was IgM positive, with all three diagnostic IgM bands reported.²

When testing was repeated one week later, the patient remained IgM positive and had developed an IgG response meeting the criteria used by the authors. This IgG seroconversion provided additional evidence supporting recently acquired Lyme disease.²

The patient was treated with IV ceftriaxone and doxycycline for four weeks. His neurological function subsequently improved. He was eventually weaned from ventilator support, and eight months after symptom onset he had regained full upper-extremity strength, with only mild residual lower-extremity weakness and paresthesia.²

This case is particularly important because Lyme neuroborreliosis did not simply resemble GBS clinically. The spinal fluid, MRI, and electrodiagnostic studies also supported a GBS-like demyelinating process. The authors concluded that the pattern suggested demyelination secondary to Lyme neuroborreliosis rather than an unrelated coincidental Guillain-Barré syndrome.²

How Can Lyme Neuroborreliosis and GBS Be Distinguished?

No single symptom or test necessarily distinguishes Lyme neuroborreliosis from Guillain-Barré syndrome. The entire clinical picture matters.

Potential clues favoring Lyme neuroborreliosis may include:

• Severe radicular or nerve-root pain
• Facial palsy, particularly bilateral facial involvement
• Other cranial neuropathies
• CSF lymphocytic pleocytosis
• Possible tick exposure
• Outdoor activity in tick habitat
• Residence in or travel to a Lyme-endemic area
• Erythema migrans or another compatible rash
• Compatible Lyme serology and CSF findings

However, these clues are not absolute. The 2023 case is particularly instructive because the patient’s CSF contained no white blood cells and instead showed albuminocytologic dissociation, which initially favored GBS.²

The absence of a recognized tick bite or rash also does not rule out Lyme disease. Neither patient described in these reports recalled a definite tick bite.

Guillain-Barré syndrome remains a neurological emergency. Progressive weakness, difficulty walking, facial weakness, swallowing difficulty, or breathing problems require urgent medical evaluation rather than assuming the symptoms are caused by Lyme disease.

Why These Two Cases Matter

The 2023 and 2026 cases demonstrate two different ways Lyme neuroborreliosis can resemble Guillain-Barré syndrome.

In the 2023 case, the resemblance was unusually strong. The patient had ascending weakness, areflexia, albuminocytologic dissociation, cauda equina enhancement, and electrodiagnostic evidence of demyelination. His illness progressed to respiratory failure despite treatment with IVIG before Lyme disease was identified and treated.²

In the 2026 case, weakness, reduced reflexes, paresthesias, and bilateral facial palsy also initially raised concern for GBS. However, severe radicular pain and substantial CSF pleocytosis provided important clues pointing toward Lyme meningoradiculitis and Bannwarth syndrome.¹

Together, the cases illustrate an important principle: similar neurological symptoms can arise from different disease processes, and Lyme neuroborreliosis should not be diagnosed—or excluded—on the basis of one symptom or one test alone.

Frequently Asked Questions

Can Lyme disease mimic Guillain-Barré syndrome?

Yes. Lyme neuroborreliosis can rarely produce weakness, numbness, reduced reflexes, facial palsy, radicular pain, and other neurological findings that resemble Guillain-Barré syndrome.

Can Lyme neuroborreliosis look like GBS on nerve testing?

It can in rare cases. In one reported patient, nerve conduction studies showed prolonged distal motor latency, conduction block, and absent F-wave responses consistent with an acute demyelinating polyneuropathy. These findings contributed to the initial diagnosis of Guillain-Barré syndrome.²

What is Bannwarth syndrome?

Bannwarth syndrome is a neurological manifestation of Lyme borreliosis involving painful inflammation of the meninges and nerve roots. It may cause severe radicular pain, sensory symptoms, weakness, and cranial neuropathies such as facial palsy.

Can Lyme disease cause severe back or nerve pain?

Yes. Lyme neuroborreliosis can cause radiculitis or meningoradiculitis, producing severe nerve-root pain that may radiate from the back into the chest, abdomen, arms, or legs.

Can Lyme neuroborreliosis occur without a rash or known tick bite?

Yes. The absence of a recognized erythema migrans rash or known tick bite does not exclude Lyme neuroborreliosis. Exposure history, neurological findings, laboratory testing, spinal fluid findings, and other clinical evidence may all contribute to the diagnosis.

Does Lyme neuroborreliosis always cause white blood cells in spinal fluid?

No. CSF pleocytosis is commonly associated with Lyme neuroborreliosis, but the 2023 case described here had no CSF white blood cells and instead showed elevated protein with albuminocytologic dissociation, closely resembling the spinal fluid pattern associated with Guillain-Barré syndrome.²

Clinical Takeaway

Guillain-Barré syndrome is a serious neurological emergency, but Lyme neuroborreliosis can occasionally produce a remarkably similar clinical picture.

The two cases illustrate different diagnostic challenges. One patient had prominent radicular pain and inflammatory spinal fluid that ultimately pointed toward Bannwarth syndrome. The other had ascending paralysis, albuminocytologic dissociation, cauda equina enhancement, and demyelinating nerve conduction findings that closely resembled classic GBS.^1,2

When weakness and reduced reflexes occur together with facial palsy, radicular pain, cranial neuropathies, a compatible exposure history, or other evidence suggesting Lyme disease, Lyme neuroborreliosis may deserve consideration in the differential diagnosis.

At the same time, rapidly progressive weakness, swallowing difficulty, or respiratory symptoms require urgent evaluation because Guillain-Barré syndrome and other neurological disorders can become life-threatening.

Related Articles

Learn more about neurologic Lyme disease, facial palsy, nerve symptoms, and conditions that may resemble Lyme disease:

Neurologic Lyme Disease

Can Lyme Disease Cause Bilateral Facial Palsy?

Lyme Disease Misdiagnosis: Why It Happens and What to Know

Can a Tick Bite Cause Guillain-Barré Syndrome?

Neurologic Lyme Disease Misdiagnosed as Conversion Disorder

References

1. Bhattarai A, Kaur M, Valaparla V, Li X. A Rare Case of Lyme Neuroborreliosis Presenting as Bannwarth Syndrome in Texas. Cureus. 2026;18(5):e109422. doi:10.7759/cureus.109422.
2. Farr J, Bittar J. Neuroborreliosis Presenting as Guillain-Barré Syndrome. Cureus. 2023;15(7):e42322. doi:10.7759/cureus.42322.
3. National Institute of Neurological Disorders and Stroke. Guillain-Barré Syndrome.
4. Cleveland Clinic. Guillain-Barré Syndrome.

This article is for educational purposes and is not intended to provide medical advice. New or rapidly progressive weakness, facial paralysis, difficulty swallowing, or breathing difficulty requires prompt medical evaluation.

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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