Lyme Disease Mimicking Spinal Cord Infarct: A Diagnostic Challenge

Severe neurologic symptoms developed rapidly
Imaging suggested spinal cord infarction
Lyme disease was ultimately identified and treated

In their article, “Dueling etiologies: longitudinally extensive spinal cord lesion mimicking infarct,” Kalaszi and colleagues describe a complex case where Lyme disease was considered as a potential cause of a severe spinal cord lesion.

The patient had reported a bull’s-eye rash 6 months before symptom onset, raising suspicion for Lyme disease. :contentReference[oaicite:0]{index=0}

Rapid Neurologic Decline

The man presented with chest pain followed by progressive weakness in the right lower limb. His symptoms were preceded by 2 weeks of constipation and voiding dysfunction—features suggestive of early autonomic involvement.

He rapidly developed:

• Bilateral flaccid paralysis of the lower limbs
• Absent knee and ankle reflexes
• Sensory abnormalities
• Urinary retention and reduced anal tone

These symptoms reflect patterns seen in Lyme disease symptoms, particularly when the nervous system is involved.

Imaging Suggested Spinal Cord Infarction

MRI of the brain and spine revealed an extensive abnormal signal from the T4 level to the conus medullaris.

The findings were consistent with longitudinally extensive transverse myelitis (LETM), with possible causes including autoimmune, paraneoplastic, or infectious processes.

Spinal cord infarction was also considered, as many patients present with sudden pain followed by neurologic deficits.

Evidence Supporting Lyme Disease

Further testing revealed intrathecal IgG antibodies against Borrelia antigens (p21 and VlsE), supporting Lyme neuroborreliosis.

These findings align with broader patterns described in neurologic Lyme disease, where central nervous system involvement can produce diverse presentations.

The patient was treated with intravenous ceftriaxone.

A Complicating Finding: Amphiphysin Antibodies

Testing also revealed amphiphysin antibodies, which are associated with paraneoplastic and autoimmune neurologic syndromes.

However, extensive evaluation—including PET imaging—did not reveal malignancy.

This raised the possibility of overlapping or competing etiologies.

Clinical Recovery

The patient was treated with corticosteroids and 3 weeks of intravenous ceftriaxone.

Over time, he improved significantly:

• Able to walk with a stick after 6 weeks
• Recovery of bowel and bladder function

Why This Matters

This case highlights how Lyme disease can mimic serious neurologic conditions, including spinal cord infarction and transverse myelitis.

Autonomic symptoms—such as constipation and urinary dysfunction—may precede more severe neurologic deficits, as seen in autonomic dysfunction in Lyme disease.

When patients present with unexplained spinal cord lesions or rapidly evolving neurologic symptoms, Lyme disease should remain part of the differential diagnosis—especially when there is a history of rash or exposure risk.

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