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Neurological Lyme disease

Lyme Disease

Neurological Lyme disease symptoms may be due to an autoimmune dysfunction.
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Lyme disease is a tick-borne illness caused by an infection with Borrelia burgdorferi, a spiral-shaped bacteria, which can be transmitted through the bite of an infected blacklegged (or deer) tick. Once the tick is attached to its host, it feeds on the blood, releasing bacteria into the bloodstream. The bacteria (or spirochete) disseminate throughout the body and lodge in soft tissues and organs, including the heart, brain, central nervous system, joints and muscles. And in some cases, Lyme disease can cause debilitating neurological and psychiatric symptoms.

Lyme disease is diagnosed based on clinical symptoms, medical history and exposure to ticks. According to the CDC, there are several objective signs of Lyme disease, including Bell’s palsy, synovitis of the knee, and the presence of an erythema migrans (or bull’s-eye) rash.

Symptoms can vary from person to person. Initially, individuals typically develop flu-like symptoms including fatigue, fever, chills, headaches, joint and muscle pain and swollen lymph nodes. However, Lyme disease can also cause numerous neurologic and psychiatric manifestations, as well.

Lyme disease triggers autoimmune-induced neurological symptoms

Numerous studies indicate that a persistent, chronic infection with Borrelia burgdorferi (the causative agent of Lyme disease) can cause a range of psychiatric and neurologic issues. In some cases, chronic neurological Lyme disease symptoms may be due to an infection-triggered autoimmune response.

One study found elevated levels of autoimmune antibodies in Lyme disease patients with persistent psychiatric and neurological symptoms, suggesting an underlying autoimmune etiology. 1 Investigators also report that “anxiety, depression, panic attacks, hallucinations, delusions and pain … are common among patients who report a [tick-borne disease] diagnosis.” 2

  Up to 40% of Lyme disease patients experience neurological symptoms. 3

Patients with chronic symptoms often suffer from neurological complications. In fact, neurological involvement has been reported in up to 40% of patients with Lyme disease, while depressive episodes occurred in up to 66% of patients. 3 Cognitive complaints occur in up to 90% of individuals with chronic Lyme disease symptoms. 4

Additionally, some children with Lyme disease have been reported as having “substantial cognitive and psychiatric disturbances.” Meanwhile, Lyme disease in adults has been associated with a range of psychiatric conditions including paranoia, dementia, schizophrenia, bipolar disorder, panic attacks, major depression, anorexia nervosa, and obsessive-compulsive disorder. 3

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Chronic neurological Lyme disease symptoms due to autoimmune dysfunction

While many Lyme disease patients will improve with appropriate antibiotic therapy, others may experience ongoing neurological and/or psychiatric symptoms – that are not responsive to treatment. These chronic symptoms can include a broad range of neuropsychiatric manifestations and cognitive decline. 5

Several studies indicate that Lyme disease can trigger an autoimmune dysfunction resulting in chronic neuropsychiatric symptoms. How does this happen? An infection with Borrelia burgdorferi (the bacteria which causes Lyme disease) can ignite an autoimmune response, whereby antibodies meant to attack the harmful bacteria mistakenly attack healthy tissue in an area of the brain known as the basal ganglia. This misdirected attack leads to brain inflammation and disrupts how cells and receptor’s function, resulting in neurologic and/or psychiatric symptoms. 5

Testing with the Autoimmune Brain Panel™ can assist clinicians in identifying whether chronic psychiatric and neurological Lyme disease symptoms may be due to an underlying autoimmune process. One study found elevated levels of antineuronal antibodies (as measured with the Autoimmune Brain Panel™) were associated with persistent symptoms of Lyme disease in patients with repeat Borrelia infections. 6

The authors suggest that “elevated anti-Lysoganglioside antibody levels [as measured with the Panel] may play a role in symptom persistence.” This finding raises the possibility that a non-infectious immune-mediated process may be inducing disease. 6

Furthermore, neurologic and neuropsychiatric symptoms may emerge, “as a result of elevated autoantibodies against anti-Lysoganglioside GM1 … and against the dopamine 1 receptor.” 6

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Can neurological Lyme be due to an immune dysfunction?

Take our quiz and see if your symptoms may be due to an underlying autoimmune dysfunction and if testing may be right for you.

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Answer a few questions to find out if you might benefit from testing with the Autoimmune Brain Panel™.

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Are you struggling with neurological Lyme disease symptoms? It may be due to an autoimmune response.

Neurological Lyme Disease before treatment
Neurological Lyme disease after treatment
Neurological Lyme symptoms before Autoimmune Brain Panel™

Testing helps identify autoimmune basis for neuropsychiatric symptoms

Six months after visiting a tick endemic region, a 7-year-old girl developed multiple neuropsychiatric symptoms. She tested positive for Lyme disease, had a history of strep infections and was previously diagnosed with PANDAS – Pediatric Autoimmune Neuropsychiatric Disorder Associated with Strep infections. 7

Despite several months of treatment with various oral and IV antimicrobial medications for Lyme disease, the patient continued to suffer from debilitating neurologic and psychiatric symptoms including OCD, aggressive behaviors, panic attacks and cognitive decline.

  Anti-Lysoganglioside antibodies [as measured with the Panel] were significantly elevated in patients with post-treatment Lyme disease symptoms. 6

She was tested with the Autoimmune Brain Panel™ (formerly known as the Cunningham Panel™) which revealed elevated levels of several antineuronal autoantibodies – indicating an underlying autoimmune response could be contributing to her chronic illness.

Based upon test results, the patient was treated with intravenous immunoglobulin (IVIg) and after 3 courses of IVIg, she experienced complete resolution of symptoms.

The presence of elevated antineuronal antibodies identified by the Autoimmune Brain Panel™ provided an aid in diagnosis of an immune-mediated neuropsychiatric condition and assisted in directing immunomodulatory treatment.

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  1. Garcia-Monco JC, Seidman RJ, Benach JL. Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides. Infect Immun. 1995 Oct;63(10):4130-7. doi: 10.1128/iai.63.10.4130-4137.1995. PMID: 7558329; PMCID: PMC173580. https://pubmed.ncbi.nlm.nih.gov/7558329/
  2. Maxwell, S.P.; Brooks, C.; McNeely, C.L.; Thomas, K.C. Neurological Pain, Psychological Symptoms, and Diagnostic Struggles among Patients with Tick-Borne Diseases. Healthcare 2022, 10, 1178. https://doi.org/10.3390/healthcare10071178
  3. Fallon BA, Nields JA: Lyme disease: a neuropsychiatric illness. Am J Psychiatry. 1994, 151:1571-83. 10.1176/ajp.151.11.1571. https://pubmed.ncbi.nlm.nih.gov/7943444/
  4. Touradji P, Aucott JN, Yang T, Rebman AW, Bechtold KT. Cognitive Decline in Post-treatment Lyme Disease Syndrome. Arch Clin Neuropsychol. 2019 Jun 1;34(4):455-465. doi: 10.1093/arclin/acy051. PMID: 29945190. https://academic.oup.com/acn/article/34/4/455/5045218
  5. Rebman AW, Aucott JN. Post-treatment Lyme Disease as a Model for Persistent Symptoms in Lyme Disease. Front Med (Lausanne). 2020 Feb 25;7:57. doi: 10.3389/fmed.2020.00057. PMID: 32161761; PMCID: PMC7052487. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7052487/
  6. Brian A. Fallon, Barbara Strobino, Sean Reim, Julie Stoner, Madeleine W. Cunningham, Anti-lysoganglioside and other anti-neuronal autoantibodies in post-treatment Lyme Disease and Erythema Migrans after repeat infection, Brain, Behavior, & Immunity – Health, 2020,100015,ISSN 2666-3546, https://doi.org/10.1016/j.bbih.2019.100015
  7. Cross A., Bouboulis D., Shimasaki C., Jones C.R. Case Report: PANDAS and Persistent Lyme Disease With Neuropsychiatric Symptoms: Treatment, Resolution, and Recovery. Front. Psychiatry, 02 February 2021 | https://doi.org/10.3389/fpsyt.2021.505941
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