Encephalitis of the brain can trigger changes in behavior
Autoimmune encephalitis (AE) occurs when the body’s immune system produces antibodies that mistakenly attack the brain. These autoantibodies target receptors or proteins in different regions of the brain, which can result in a range of neuropsychiatric symptoms. 1
In recent years, the number of confirmed cases of AE [autoimmune encephalitis] has been increasing annually, as a growing number of neuronal autoantibodies are discovered. 2
There are different forms of autoimmune encephalitis, each defined by the antibodies involved and the targets within the brain. Basal ganglia encephalitis can occur when autoantibodies attack an area of the brain known as the basal ganglia. PANS and PANDAS are a subtype of basal ganglia encephalitis. 3
Basal ganglia encephalitis, which is frequently caused by an underlying infection, can trigger neurologic and psychiatric symptoms, such as obsessions/compulsions, anxiety, depression, mood swings and other changes in behavior. 3
It is critical to identify whether psychiatric symptoms, neurologic manifestations or a change in behavior or personality is due to an autoimmune encephalopathy rather than a primary psychiatric illness, since treatment requires a different approach. And, with the proper treatment, symptoms can be greatly reduced or completely resolved.
Treatment includes: identifying and eradicating the infections, treating the immune system dysfunction and reducing inflammation or encephalitis of the brain. This typically involves immunomodulatory therapies, such as anti-infective medications, antibiotics, anti-inflammatory drugs, steroids, IVIG or plasmapheresis. 4
What to Look For
Individuals with neuropsychiatric symptoms associated with an infection-triggered basal ganglia encephalitis typically have a medical history which includes several of the following:
- New onset of symptoms at an age that is not typical for that condition. For example, late-onset OCD or early-onset bipolar disorder .
- Symptoms may appear suddenly (but not always).
- Medications may not be effective or may make symptoms worse.
- Personal or family history of autoimmune diseases. These diseases may include diabetes, lupus, rheumatoid arthritis and many others.
- Family member or close relative has been diagnosed with Rheumatic Fever.
- Changing diagnoses or multiple diagnoses.
- The presence of other neurologic (tics, urinary problems, sleep disturbances) or psychiatric symptoms.
- Onset of symptoms following infection(s).
- Current, or past history of an infection(s).
Infections may be subclinical, meaning they may not produce outward, physical symptoms. Yet, these “hidden” and unidentified infections may still trigger an autoimmune reaction, resulting in neurologic and/or psychiatric symptoms.
Neuropsychiatric symptoms return after stopping treatment. A patient may have been treated for an infection and physical symptoms resolved. However, shortly after stopping the medication, neuropsychiatric symptoms return.
If behavioral, neurologic or psychiatric symptoms are reduced/disappear with antibiotic treatment but re-appear when treatment is stopped, the symptoms may be due to an autoimmune encephalopathy.
The term “encephalitis,” which is inflammation of the brain, can create the misperception that a person with this condition is seriously disabled and their illness is obvious. This is not always the case. Up to 60% of cases remain undiagnosed. 5
Patients with an autoimmune-induced encephalitis may exhibit behavior or personality changes but are still able to function.
Why is it important to identify whether neuropsychiatric symptoms are caused by an infection-triggered autoimmune encephalopathy?
- Treatment is different and often involves anti-infective and immunomodulatory therapies.
- Early diagnosis and treatment has been shown to improve chances for a full recovery.
- With proper treatment, symptoms/behaviors are often resolved with significant improvement in symptoms or a complete remission.
- Platt MP, Agalliu D, Cutforth T. Hello from the Other Side: How Autoantibodies Circumvent the Blood-Brain Barrier in Autoimmune Encephalitis. Front Immunol. 2017;8:442. Published 2017 Apr 21. doi:10.3389/fimmu.2017.00442
- Gu Y, Zhong M, He L, et al. Epidemiology of Antibody-Positive Autoimmune Encephalitis in Southwest China: A Multicenter Study. Front Immunol. 2019;10:2611. Published 2019 Nov 12. doi:10.3389/fimmu.2019.02611
- Chain JL, Alvarez K, Mascaro-Blanco A, et al. Autoantibody Biomarkers for Basal Ganglia Encephalitis in Sydenham Chorea and Pediatric Autoimmune Neuropsychiatric Disorder Associated With Streptococcal Infections. Front Psychiatry. 2020;11:564. Published 2020 Jun 24. doi:10.3389/fpsyt.2020.00564
- Jennifer Frankovich, Susan Swedo, Tanya Murphy, Russell C. Dale, Dritan Agalliu, Kyle Williams, Michael Daines, Mady Hornig, Harry Chugani, Terence Sanger, Eyal Muscal, Mark Pasternack, Michael Cooperstock, Hayley Gans, Yujuan Zhang, Madeleine Cunningham, Gail Bernstein, Reuven Bromberg, Theresa Willett, Kayla Brown, Bahare Farhadian, Kiki Chang, Daniel Geller, Joseph Hernandez, Janell Sherr, Richard Shaw, Elizabeth Latimer, James Leckman, Margo Thienemann, and PANS/PANDAS Consortium.Journal of Child and Adolescent Psychopharmacology.Sep 2017.574-593.http://doi.org/10.1089/cap.2016.0148
- National Institute of Neurologic Disorders and Stroke