Lyme Disease Mistaken for Dementia: When Confusion Is Reversible

Confusion and memory loss in older adults may be mistaken for dementia.
Lyme neuroborreliosis can cause reversible cognitive decline when treated early.
Spinal fluid findings and CXCL13 may help distinguish infection from neurodegeneration.

Can Lyme disease mimic dementia? Yes. In some cases, confusion, memory loss, and behavioral changes may be due to Lyme neuroborreliosis — not a primary neurodegenerative condition.

This case highlights how symptoms initially attributed to dementia were ultimately reversible with antibiotic treatment — and why infectious causes deserve consideration in patients with atypical or rapidly progressive cognitive decline.

For a broader overview of how Lyme disease affects the brain, see Lyme encephalopathy symptoms and complications.

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Initial Presentation: Suspected Dementia

An 80-year-old man presented with confusion and disorientation, reduced attention and concentration, short-term memory impairment, increased motor activity, and mild thought disorder including some tangential thinking — but without frank psychotic symptoms.

He was diagnosed with delirium, possibly related to early dementia. An abnormal FDG-PET scan was interpreted as consistent with early Alzheimer’s disease, and memantine was prescribed.

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Worsening Symptoms Despite Treatment

The patient’s condition did not improve with dementia-directed treatment.

Despite receiving the antipsychotic medications risperidone and pipamperone for sleep disturbances, he remained confused. He developed persistent disorientation, recurrent sleep-wake cycle disturbances, intermittent restlessness, and incontinence.

The failure to respond to standard dementia and psychiatric treatment prompted further investigation.

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Clues to an Alternative Diagnosis

A spinal tap revealed findings inconsistent with primary neurodegeneration:

• Elevated protein
• Lymphocytic pleocytosis of 260 cells per microliter
• Intrathecal IgM synthesis
• Elevated lactate

The lymphocytic pleocytosis with signs of immune activation and the dominance of intrathecal IgM synthesis shifted the differential diagnosis toward neurologic Lyme disease — specifically neuroborreliosis.

These findings suggested an active inflammatory or infectious process rather than a primary degenerative condition.

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A Potential Biomarker: CXCL13

The patient also had elevated cerebrospinal fluid CXCL13 levels.

Although not yet validated as a routine diagnostic tool, CSF CXCL13 may help increase diagnostic sensitivity and accuracy in central nervous system manifestations of Lyme disease — alongside lymphocytic pleocytosis — in cases where standard testing is inconclusive.

This emerging biomarker may eventually improve detection of neuroborreliosis in patients whose presentations overlap with neurodegeneration.

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Treatment and Recovery

The patient was treated with intravenous ceftriaxone for 21 days.

Following treatment, his confusion and delirious symptoms resolved. He was discharged in clearly improved clinical status — despite an additional complication of aspiration pneumonia during his hospitalization.

This outcome demonstrates that symptoms resembling dementia may be reversible when caused by an underlying infection that is recognized and treated appropriately.

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Why Lyme Disease Can Be Missed in Older Adults

Neuroborreliosis can closely mimic dementia, delirium, and psychiatric disorders — particularly in older adults where cognitive decline is more readily attributed to neurodegeneration.

Several factors contribute to missed diagnosis:

• Nonspecific cognitive and behavioral symptoms
• Overlap with Alzheimer’s disease and other dementias
• Reliance on imaging findings without full clinical context
• Failure to consider infectious etiology in older patients

In this case, an abnormal FDG-PET scan initially supported an Alzheimer’s diagnosis — illustrating how imaging findings can mislead when an underlying infection is not considered.

Blanc and colleagues identified a series of patients with Lyme neuroborreliosis who were initially diagnosed with dementia syndromes, finding that cognitive symptoms improved following antibiotic treatment in a subset of cases.

A 2024 review confirmed that Lyme neuroborreliosis should be considered in the differential diagnosis of dementia syndromes — particularly in endemic areas and when standard dementia treatments fail to produce improvement.

These challenges parallel broader issues discussed in Lyme disease misdiagnosis.

For a broader overview of the Lyme disease and dementia overlap — including additional clinical cases and what the research shows — see Lyme Disease and Dementia: When Cognitive Decline Has Another Cause.

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Frequently Asked Questions

Can Lyme disease cause symptoms that look like dementia?

Yes. Lyme neuroborreliosis can cause confusion, memory loss, disorientation, and behavioral changes that closely resemble dementia — particularly in older adults.

How can doctors distinguish Lyme encephalopathy from dementia?

Spinal fluid analysis may reveal inflammatory findings such as lymphocytic pleocytosis and intrathecal IgM synthesis that suggest infection rather than neurodegeneration. Elevated CSF CXCL13 may also support a diagnosis of neuroborreliosis.

Can Lyme-related cognitive symptoms be reversed?

In some cases, yes. This case demonstrates that confusion and delirium attributed to dementia resolved following a 21-day course of intravenous ceftriaxone — highlighting the importance of considering infectious causes before assuming a neurodegenerative diagnosis.

Should Lyme disease be tested for in patients with dementia?

When dementia symptoms are atypical, rapidly progressive, or fail to respond to standard treatment — particularly in Lyme-endemic areas — testing for neuroborreliosis is clinically reasonable and may prevent missed treatable diagnoses.

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Clinical Takeaway

Lyme disease can mimic dementia — but unlike primary neurodegeneration, infection-related cognitive decline may be reversible with appropriate antibiotic treatment. In this case, an 80-year-old man whose confusion was initially attributed to Alzheimer’s disease recovered significantly following intravenous ceftriaxone.

In patients with atypical, rapidly progressive, or treatment-resistant cognitive decline — particularly in Lyme-endemic areas — infectious causes including neuroborreliosis deserve consideration before a degenerative diagnosis is assumed.

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Related Articles

• Lyme Encephalopathy Symptoms and Complications
• Lyme Disease and Dementia: When Cognitive Decline Has Another Cause
• Lyme Disease or Dementia? A Case of Reversible Cognitive Decline
• Lyme Disease Misdiagnosis
• Neurologic Lyme Disease
• Brain Fog in Lyme Disease

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References

1. Karrasch M, Fingerle V, Boden K, Darr A, Baier M, Straube E, Nenadic I. Neuroborreliosis and acute encephalopathy: The use of CXCL13 as a biomarker in CNS manifestations of Lyme borreliosis. Ticks Tick Borne Dis. 2018;9(2):415-417.
2. Sanchini C, Papia C, Cutaia C, Poloni TE, Cesari M. A case of reversible dementia? Dementia vs delirium in Lyme disease. Ann Geriatr Med Res. 2023;27(1):80-82.
3. Bashchobanov DH, Stamatova E, Andonova R, Dragusheva E, Gadzhovska V, Popov G. Lyme neuroborreliosis in the context of dementia syndromes. Cureus. 2024;16(8):e67057.
4. Blanc F, Philippi N, Cretin B, et al. Lyme neuroborreliosis and dementia. J Alzheimers Dis. 2014;41(4):1087-1093.

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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