Peripheral Monocytes and Soluble Biomarkers in Autoimmune Encephalitis
Written in plain language for patients to easily understand.
For this research, we set out to find out answers to following –
- Are monocytes in people with AE different than in healthy people?
- Is there other evidence of inflammation in the blood of people with AE?
- Does the level of inflammation in AE determine disease severity?
- Are the inflammatory changes the same in different types of AE?
This article goes over how the researchers did the work, the interesting things they found, and what those finding mean.
Psychiatric Manifestations of Autoimmune Encephalitis
Written in plain language for patients to easily understand.
Why we did this work
Autoimmune encephalitis is a disorder in which antibodies accidentally created by the immune system attack parts of the brain. This can lead to inflammation and nerve damage.
Psychiatric problems are common in autoimmune encephalitis and can imitate mental health conditions, for example psychotic illnesses like schizophrenia. It is important to separate patients with AE from those with mental illness as treatments are very different.
There are different subtypes of AE. Some cases are due to the presence of detectable auto antibodies (a protein targeting the person’s own nerve endings) which is known as ‘sero positive’ AE. In ‘sero negative’ AE, there is no detectable antibody when using currently available techniques for detection.
Within the ‘sero positive’ group are different AE categories depending on the type of antibody. Nine types of AE are discussed further in the next section. Diagnosis and red flags are covered.
Cognition in Autoimmune Encephalitis
Written in plain language for patients to easily understand. A background about AE is provided with an explanation of how symptoms fluctuate and patients differ. The current tool to measure how a patient is doing in their daily lives does not sufficiently show the deficits. The group gathered cognitive data from patients
previously diagnosed with autoimmune
encephalitis and explain their findings.
An overview of N-methyl D-asparate receptor (NMDAR) antibody-associated encephalitis
Written in plain language for patients to easily understand. A brief explanation of anti-NMDAR, its symptoms, and diagnostic process are reviewed.
Anti-NMDAR encephalitis can be treated using medications that selectively reduce components of the immune system, but as the illness is different from person to person, it is challenging to both diagnose and manage. The use of biological markers, or biomarkers (proteins, cells, or other characteristics that can generally be detected via a certain test and are associated with a particular disease), may be particularly useful for the diagnosis and assessment of how effective treatment is to manage a patient’s illness. Accurate and specific biomarkers for anti-NMDAR encephalitis still do not exist. The summary goes over what they discovered.
EPILEPSY AND AUTOIMMUNE ENCEPHALITIS
This summary is written in plain language for patients to easily understand.
While some patients will stop having seizures after immune system suppressing treatment, others will continue to have seizures that do not respond, even to increasing amounts of anti-seizure medications. This is known clinically as treatment- or drug-resistant epilepsy. Drug-resistant epilepsy has a significant impact on the quality of life of people with autoimmune encephalitis. We currently do not know why some patients with autoimmune encephalitis develop drug-resistant epilepsy whilst others do not.
It is important for doctors to be able to predict how and why people with autoimmune encephalitis develop drug-resistant epilepsy because it is a disabling complication that may be preventable. For this research, we wanted to find out answers to the following questions –
- How common is drug-resistant epilepsy after autoimmune encephalitis?
- What are the risk factors for the development of drug-resistant epilepsy after autoimmune encephalitis?
- In the early part the disease, can the use of EEG tell us about a person’s likelihood of developing drug-resistant epilepsy?
- Can we use this information to predict which patients with autoimmune encephalitis are going to develop drug resistant epilepsy?
Using Electroencephalogram for quicker diagnosis and prediction of the likely course for patients with Autoimmune Encephalitis
This summary is written in plain language for patients to easily understand. Patients thought to have autoimmune encephalitis usually have a few clinical tests to confirm the diagnosis. It is important for patients with suspected autoimmune encephalitis to have a diagnosis as soon as possible because earlier treatment leads to better long-term recovery. But doing multiple clinical tests takes time, some can be invasive or may only be available in certain centers.
Researchers looked into these questions: Can we use an EEG to identify different types of Autoimmune Encephalitis?
– In the early part of the disorder, can the
EEG tell us about a person’s likely
course in the long-term (outcomes)?
Monash researchers explain how they did the work and what they found.
RARE & SERONEGATIVE AUTOIMMUNE ENCEPHALITIS
This summary is written in plain language for patients to easily understand. In up to half of cases, an antibody is not detectable using currently available tests or assays. This group of cases is called “seronegative” autoimmune encephalitis.
However, seronegative autoimmune encephalitis remains less well characterized, possibly in part because of its heterogeneous nature – meaning that a variety of diseases forms may be included by the definition.
The purpose of our review was to explore advances regarding five rare antibody-mediated forms of autoimmune encephalitis, namely, anti-g-aminobutyric acid B (GABAB) receptor-, anti-a-amino-3hydroxy-5-methyl-4-isoxazolepropinoic receptor- (AMPAR), anti-GABAA receptor-and anti-dipeptidyl-peptidase-like protein-6 (DPPX) encephalitis and IgLON5 disease.
Researchers also summarise current research and challenges in relation to ‘seronegative’ autoimmune encephalitis.