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Nov 06

Could Lyme disease have led to a spinal cord lesion?

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Can Lyme Disease Cause Lesions on the Spine?

Lyme neuroborreliosis has rarely been associated with spinal cord lesions
One patient developed a longitudinally extensive spinal cord abnormality
He improved following steroids, IV ceftriaxone, and rehabilitation

Can Lyme disease cause lesions on the spine? Lyme neuroborreliosis has rarely been associated with inflammatory lesions involving the spinal cord, including transverse myelitis and myelopathy. However, spinal cord lesions have many possible causes, and the evidence in an individual case may not establish Lyme disease as the only explanation.

In their article, “Case report: Dueling etiologies: Longitudinally extensive spinal cord lesion mimicking spinal cord infarct with simultaneous positive Lyme serology and amphiphysin antibody,”1 Kalaszi and colleagues describe a 55-year-old man with a spinal cord lesion and several competing diagnostic possibilities.

The man reported an insect bite accompanied by a bull’s-eye-like rash approximately 6 months before the onset of his neurologic illness. His subsequent testing raised the possibility of Lyme neuroborreliosis as one contributor to the spinal cord lesion.

Sudden weakness and autonomic dysfunction

The patient presented with chest pain followed by weakness in his right lower limb. During the preceding 2 weeks, he had experienced constipation and difficulty urinating.

His condition deteriorated over the next 24 hours. He developed severe flaccid weakness in both legs, absent knee and ankle reflexes, abnormal plantar responses, patchy sensory impairment, urinary retention, and reduced anal tone.

These findings indicated substantial dysfunction involving the spinal cord and the nerves controlling his legs, bowel, and bladder.

MRI revealed an extensive spinal cord lesion

MRI of the brain and entire spine revealed an abnormal increased T2 signal along the anterior portion of the spinal cord. The abnormality extended from the T4 level to the conus, without associated swelling or contrast enhancement.

Because the lesion involved more than three vertebral segments, it was classified as a longitudinally extensive spinal cord lesion. The physicians considered several potential explanations, including:

  • Spinal cord infarction
  • Longitudinally extensive transverse myelitis
  • Lyme neuroborreliosis
  • Autoimmune or paraneoplastic myelopathy

The sudden onset of chest pain and weakness, along with the location and appearance of the MRI abnormality, initially supported spinal cord infarction.

Symptoms of spinal cord infarction depend on the affected region of the spinal cord and often develop suddenly. According to the authors, approximately 70% of patients report acute back, chest, neck, or limb pain before the neurologic deficit appears.

Could Lyme disease explain the spinal cord lesion?

The patient’s history included a bull’s-eye-like rash approximately 6 months before his neurologic presentation. He had also developed bowel and bladder dysfunction during the 2 weeks before the acute weakness.

His initial Lyme C6 antibody screening test was strongly positive, but the confirmatory serum immunoblot was negative. His cerebrospinal fluid did not have the elevated white blood cell count typically found in active Lyme neuroborreliosis.

However, additional cerebrospinal fluid testing detected intrathecal immunoglobulin G antibodies directed against two Borrelia-specific antigens, p21 and VlsE. These findings again raised the possibility that Lyme neuroborreliosis contributed to the spinal cord disease.

Lyme-associated myelitis is uncommon, but previous case reports have described transverse myelitis and longitudinally extensive spinal cord lesions in patients with neuroborreliosis.

A second abnormal finding complicated the diagnosis

The patient also tested positive for amphiphysin antibodies. These antibodies are commonly associated with paraneoplastic neurologic syndromes, including stiff-person syndrome, encephalomyelitis, dysautonomia, and myelopathy.

In a series described by Moon and colleagues, the most common neurologic manifestation among patients with non-stiff anti-amphiphysin syndrome was limbic encephalitis, followed by dysautonomia and cerebellar dysfunction.2

CT and PET imaging did not identify a malignancy during the patient’s hospitalization. However, the absence of a detectable tumor on the initial evaluation did not completely exclude a paraneoplastic process. Amphiphysin antibodies can precede the detection of an underlying malignancy, making continued surveillance important.

Improvement following treatment

The patient improved rapidly after receiving intravenous steroids. Because Lyme neuroborreliosis remained a possible contributor, he was also treated with a 21-day course of intravenous ceftriaxone.

He continued to improve with treatment and rehabilitation. After 4 weeks, he could walk with a frame and had only mild residual weakness in his right leg.

“After 6 weeks, he was able to walk unaided with a stick, and bowel and bladder functions were fully recovered,” wrote the authors.

Because steroids, ceftriaxone, and rehabilitation were used during the same period, the patient’s recovery does not identify which treatment addressed the principal cause of his illness.

Why the cause remained uncertain

The authors concluded that it was impossible to determine with absolute certainty whether the patient had one cause of his spinal cord lesion or an unusual combination of vascular, infectious, and immune-mediated processes.

Several findings supported a possible Lyme-related cause, including the history of a bull’s-eye-like rash, the development of autonomic symptoms, and the detection of intrathecal antibodies against two Borrelia antigens.

Other findings supported spinal cord infarction or amphiphysin-associated myelopathy. The rapid response to steroids argued against an isolated spinal cord infarction, while the amphiphysin antibody required continued surveillance for an occult malignancy.

Frequently Asked Questions

Can Lyme disease cause lesions on the spine?

Lyme neuroborreliosis has rarely been associated with inflammatory spinal cord lesions, including myelitis and longitudinally extensive transverse myelitis. However, MRI abnormalities alone cannot establish Lyme disease as the cause.

Is a spinal cord lesion the same as spinal stenosis?

No. A spinal cord lesion is an abnormal area within or affecting the spinal cord. Spinal stenosis refers to narrowing of the spinal canal, which may compress the spinal cord or nerve roots. Lyme disease is not an established cause of degenerative spinal stenosis.

How is Lyme-associated myelitis diagnosed?

Diagnosis may include the clinical history, neurologic examination, spinal MRI, serum Lyme testing, cerebrospinal fluid analysis, and evidence of intrathecal Borrelia-specific antibody production. Other vascular, inflammatory, infectious, compressive, and neoplastic causes must also be considered.

Can a patient recover from a Lyme-associated spinal cord lesion?

Recovery is possible, but outcomes vary according to the cause, severity, timing of treatment, and extent of neurologic injury. In this case, the patient recovered bowel and bladder function and was able to walk with a stick after treatment and rehabilitation.

Clinical Takeaway

This case illustrates the difficulty of determining the cause of an extensive spinal cord lesion when vascular, infectious, and immune-mediated findings overlap.

Lyme neuroborreliosis was considered because of the earlier bull’s-eye-like rash, autonomic symptoms, and intrathecal antibodies against Borrelia antigens. At the same time, the MRI pattern suggested spinal cord infarction, and the amphiphysin antibody raised concern for an autoimmune or paraneoplastic disorder.

Lyme disease should remain in the differential diagnosis of an otherwise unexplained spinal cord lesion when the exposure history, clinical presentation, and laboratory findings support possible neuroborreliosis—but competing causes must be investigated carefully.

Related Articles

Podcast: Transverse myelitis and Lyme disease
Tick bite leads to Guillain-Barré syndrome
Six cases of neuroinvasive Lyme disease

References

  1. Kalaszi M, Donlon E, Ahmad MW, Mohamed AS, Boers P. Case report: Dueling etiologies: Longitudinally extensive spinal cord lesion mimicking spinal cord infarct with simultaneous positive Lyme serology and amphiphysin antibody. Front Neurol. 2022;13:905283.
  2. Moon J, Lee ST, Shin JW, et al. Non-stiff anti-amphiphysin syndrome: Clinical manifestations and outcome after immunotherapy. J Neuroimmunol. 2014;274(1-2):209-214.

Dr. Daniel Cameron, MD, MPH
Lyme disease clinician with over 30 years of experience and past president of ILADS.

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1 thought on “Could Lyme disease have led to a spinal cord lesion?”

  1. We know that Borrelia burgdorferi can pass the blood brain barrier and may cause Lyme disease related brain lesions. It would make sense that patients might have spinal cord lesions from Lyme disease.

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