Meningitis in Lyme disease can occur with radiculitis (nerve root inflammation) causing progressive weakness, severe lancinating pain, tremor, emotional lability, depression, and anxiety. A 43-year-old man developed fever, headache, neck stiffness, and photophobia but refused lumbar puncture, leading to presumptive diagnosis of viral meningitis. One month later he returned with devastating neurologic deterioration — progressive weakness, intractable radicular pain, hand tremor interfering with fine motor tasks, leg tremor causing imbalance, plus depression and anxiety. Only then was spinal tap performed, revealing CSF lymphocytic pleocytosis diagnostic for neuroborreliosis requiring IV ceftriaxone.

Inside Lyme Podcast: Meningitis and Radiculitis Case

Hello, and welcome to another Inside Lyme Podcast. I am your host Dr. Daniel Cameron. In this episode, I will be discussing a unique case involving a 43-year-old man with neurological manifestations of Lyme disease including both meningitis and radiculitis.

—

The Initial Presentation

The case was published in the journal Neurology International. According to Dabiri and colleagues, the patient had a history of “scaly erythematous macular rash on his proximal medial upper and lower extremities.”

Within two weeks he presented with a broad range of symptoms “including cough, fever, anorexia, malaise, fatigue, myalgias, cervicalgia/neck stiffness with flexion and extension, mild photophobia, headache,” the authors wrote.

This constellation of symptoms — fever, headache, neck stiffness, photophobia — is the classic triad of meningitis. Combined with the prior rash on extremities (likely erythema migrans), this presentation strongly suggests early disseminated Lyme disease with CNS involvement.

The Diagnostic Delay: Refusing Spinal Tap

The patient had extensive lab testing which revealed a mild abnormal liver function but no evidence of Lyme disease. At the onset of symptoms, the patient refused to have a spinal tap.

Doctors presumed the man suffered from viral meningitis.

The refusal of lumbar puncture created a critical diagnostic delay. Without CSF analysis, viral meningitis became the presumptive diagnosis by default. But viral meningitis and Lyme meningitis can be clinically indistinguishable — both cause fever, headache, neck stiffness, photophobia. The only way to differentiate is lumbar puncture.

Devastating Neurologic Deterioration One Month Later

One month later, the patient developed progressive weakness, severe radicular lancinating pain, emotional lability along with depression and anxiety, an occasional action tremor in hands interfering with fine motor tasks, and tremor in his legs causing imbalance and instability.

The progression from meningitis to severe radiculoneuropathy over one month represents the natural history of untreated neuroborreliosis. The symptoms expanded from central nervous system (meningitis) to peripheral nervous system (radiculitis) with devastating functional impact:

• Progressive weakness: Muscle denervation from radiculitis
• Severe lancinating pain: “Lancinating” means sharp, stabbing, electric-like pain from inflamed nerve roots
• Hand tremor: Interfering with fine motor tasks like writing, eating, dressing
• Leg tremor: Causing imbalance and instability, fall risk
• Emotional lability: Rapid mood swings, inappropriate crying or laughing
• Depression and anxiety: Both direct CNS effects and reactive to severe disability

Central and Peripheral Nervous System Involvement

Manifestations of the central nervous system (i.e., meningitis), as well as peripheral nervous system presentations (i.e., radiculitis) can occur in isolation or together.

Radiculitis or inflammation of the nerve root involving the peripheral nervous system (PNS) can lead to intractable pain, muscle denervation, and areflexia over one or a few adjacent dermatomes, wrote the authors.

This case demonstrates the full spectrum of neuroborreliosis:

• CNS involvement: Meningitis (headache, neck stiffness, photophobia, CSF pleocytosis)
• PNS involvement: Radiculitis (lancinating pain, weakness, areflexia)
• Autonomic/motor: Tremor, imbalance
• Psychiatric: Emotional lability, depression, anxiety

When both CNS and PNS are affected simultaneously, this indicates widespread dissemination of spirochetes throughout the nervous system.

The Spinal Tap That Proved the Diagnosis

At this point, results from a spinal tap were consistent with Lyme disease. “A lumbar puncture was performed, and the patient’s cerebrospinal fluid (CSF) analysis showed lymphocytic pleocytosis with white blood cell count of 225 and elevated protein of 77 and decreased glucose 38,” the authors wrote.

The CSF findings are diagnostic for bacterial or spirochetal meningitis:

• WBC 225: Markedly elevated (normal <5), indicating active CNS inflammation
• 95% lymphocytes: Lymphocytic predominance suggests viral, fungal, or spirochetal cause (bacterial meningitis shows neutrophils)
• Elevated protein (77 mg/dL): Normal is 15-45, elevation indicates breakdown of blood-brain barrier
• Decreased glucose (38 mg/dL): Normal is 50-75, low glucose suggests organisms consuming glucose or impaired glucose transport

This pattern — lymphocytic pleocytosis with elevated protein and low glucose — is classic for Lyme meningitis, distinguishing it from viral meningitis which typically has normal glucose.

Treatment and Rapid Improvement

The patient was treated with a 5-day course of doxycycline, followed by a month of intravenous ceftriaxone for meningitis and radiculitis associated with Lyme disease.

Approximately two weeks after starting treatment, the patient “noted his symptoms were significantly improved including resolution of the pain, weakness, constitutional and affective symptoms, while he still had some ambulatory difficulties.”

The rapid improvement — resolution of pain, weakness, and psychiatric symptoms within two weeks — validates the diagnosis and demonstrates the reversibility of Lyme-induced neurologic dysfunction. However, residual ambulatory difficulties indicate incomplete recovery, possibly requiring extended treatment or suggesting permanent nerve damage from the one-month delay in diagnosis.

Clinical Perspective

This case highlights the consequences of delayed diagnosis in meningitis in Lyme disease. The patient presented with classic meningitis symptoms — fever, headache, neck stiffness, photophobia — following a rash on his extremities. This should have prompted immediate Lyme testing and lumbar puncture. Instead, viral meningitis was presumed and the patient refused spinal tap.

The one-month delay allowed progression from isolated meningitis to devastating meningoradiculoneuropathy affecting both central and peripheral nervous systems. The progression demonstrates why early diagnosis and treatment matter in neuroborreliosis — delay allows irreversible nerve damage.

The psychiatric symptoms — emotional lability, depression, anxiety — are often dismissed as “stress” or “psychological reaction” to illness. But in neuroborreliosis, they can represent direct CNS involvement. The rapid resolution with antibiotics proves they were infection-driven, not primary psychiatric disease.

The tremor symptoms are particularly disabling. Hand tremor interfering with fine motor tasks affects activities of daily living — eating, writing, dressing, working. Leg tremor causing imbalance creates fall risk and limits independence. These aren’t subtle symptoms — they’re life-altering disabilities that developed because viral meningitis was presumed without confirmation.

The CSF findings deserve emphasis. The low glucose (38 mg/dL) distinguishes Lyme meningitis from viral meningitis, which typically has normal glucose. This single finding should have immediately elevated bacterial or spirochetal meningitis on the differential.

The residual ambulatory difficulties after treatment raise questions about treatment duration. One month of IV ceftriaxone is standard, but with severe radiculoneuropathy and delayed diagnosis, extended treatment might be warranted. Some patients require 6-8 weeks or longer for complete neurologic recovery.

Podcast Discussion Questions

This podcast addresses the following questions:

1. What is Lyme meningitis?
2. What is Lyme radiculitis?
3. Why is this case considered “unique”?
4. CNS and PNS manifestations can occur in isolation or together?
5. Can you discuss the patient’s symptoms of emotional lability, depression and anxiety?
6. What is the significance of the rash?
7. Initial testing for Lyme disease was inconclusive but follow-up tests were positive?
8. Any significance to MRI and spinal tap results?
9. What is the significance of a diagnosis of viral meningitis?
10. What were the other symptoms that might have helped the diagnosis?
11. Would clinical judgment to treat with antibiotics have been helpful?
12. What are your thoughts regarding the course of treatment?
13. Would it have been helpful to consider additional treatment for the remaining ambulatory difficulties?

—

Frequently Asked Questions

What is meningitis in Lyme disease?

Meningitis in Lyme disease occurs when spirochetes invade the meninges (membranes covering brain and spinal cord), causing inflammation. Symptoms include headache, neck stiffness, photophobia, and fever. CSF shows lymphocytic pleocytosis with elevated protein and often low glucose.

Can Lyme meningitis cause radiculitis?

Yes. Radiculitis (nerve root inflammation) frequently accompanies Lyme meningitis. This patient developed severe lancinating pain, progressive weakness, and areflexia from radiculitis occurring with meningitis — called meningoradiculitis.

How is Lyme meningitis different from viral meningitis?

Lyme meningitis often has low CSF glucose (this patient: 38 mg/dL), whereas viral meningitis typically has normal glucose. Both cause lymphocytic pleocytosis, making lumbar puncture essential for diagnosis. Clinical symptoms can be identical.

Can Lyme disease cause tremor?

Yes. This patient developed hand tremor interfering with fine motor tasks and leg tremor causing imbalance. Tremor in neuroborreliosis can result from cerebellar involvement, basal ganglia inflammation, or peripheral neuropathy.

Are depression and anxiety symptoms of Lyme disease?

Yes. Psychiatric symptoms including depression, anxiety, and emotional lability can represent direct CNS involvement in neuroborreliosis. This patient’s affective symptoms resolved with antibiotics, proving they were infection-driven.

Why did the patient refuse lumbar puncture initially?

The case doesn’t specify, but patients often refuse lumbar puncture due to fear of pain, paralysis, or complications. This refusal led to one month of viral meningitis presumption, allowing devastating neurologic progression.

Can ambulatory difficulties from Lyme be permanent?

Some patients have residual deficits despite treatment, particularly with delayed diagnosis. This patient still had ambulatory difficulties after one month of IV ceftriaxone, possibly requiring extended treatment or indicating permanent nerve damage from the diagnostic delay.

—

Thanks for listening to another Inside Lyme Podcast. You can read more about these cases in my show notes and on my website @DanielCameronMD.com. As always, it is your likes, comments, reviews, and shares that help spread the word about Lyme disease. Until next time on Inside Lyme.

Please remember that the advice given is general and not intended as specific advice as to any particular patient. If you require specific advice, then please seek that advice from an experienced professional.