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July 24 | Dr. Daria Muir, IAES Medical Liaison,  and (stubborn) AE survivor

The long-awaited day has arrived – Finally. It’s Monday morning, very early in the morning, and I have a flight to catch to take me to London to attend the Converging Themes in Neurology and Psychiatry conference to be held at the Royal Society of Medicine in London.  I’ve been looking forward to attending and representing IAES for so months.  I am excited.

The aim of this meeting is to review the current clinical and basic research understanding of the diagnosis and management of a range of disorders, including Autoimmune Encephalitis, Epilepsy and Dementia, that are at the interface between neurology and psychiatry.

The first day was going to be about Autoimmune Encephalitis (mainly focus on anti- NMDAr and anti-LGI1 antibodies), seen from the perspective of two neurologists (Prof. Sarosh Irani and Prof. Christopher Butler), a psychiatrist (Prof. Belinda Lennox) and an immunologist (Prof. David Wraith) and followed by some in-depths of the neuroscience of space and time, wonderfully focused on the memory process of evolution and dissolution (Prof. Eleanor Maguire), the navigation systems after long-term memory consolidation ( Prof. Hugo Spiers) and the development of hippocampal-dependent memory in humans (Prof. Faraneh Vargha-Khadem).

Ever since I got AE I started to feel uncomfortable in crowded and busy places. Too much noise and lots of conversations at the same time makes me lose focus.  Brain-fog takes over and I am lost; (this literally happened at the end of the first day, when I took the wrong bus and ended up almost outside London in the middle of the night).

But arriving at the conference and seeing the presenters and the attendants, most of them eminent names in neurology and psychiatry in the U.K., leading doctors in the field who provide care for autoimmune encephalitis patients, gave me strength to gather all my energy to attend and get the most value I could from the experience!

autoimmune encephalitis

I’ll share more in a follow up blog with a more detailed story, with slides and answers to questions.  (The AE session was the most debated one!), but now that I have returned home, I wanted to give you the “fresh flavors”, in terms of objectives that were set and reached by the speakers and take home messages:

  • NMDAR-dysfunction is the hallmark of NMDAR- antibody encephalitis and hence NMDAR antibodies
  • There are several lines of evidence (clinical evidence, immunological/epitope data, electrophysiological modeling and PET imaging)
  • Down regulation (a decrease in the number of target cells in the brain caused by NMDAR) of NMDAR is key and sufficient for disease!
  • LGI1 AE has highly distinctive clinical phenotypes
  • The disease neurobiology and the underlying immunology remain poorly understood
  • mAbs (monoclonal antibodies) can offer novel insights in terms of tools and therapies and immunology
  • Autoimmune limbic encephalitis leads to acute cognitive and behavioral disruption
  • There are persistent deficits in anterograde and remote memory after treatment
  • Hippocampal atrophy is associated with network-wide structural and functional changes
  • These changes explain memory deficits better than hippocampal volumes
  • Novel disorder of pathological tearfulness in AE requires further study
  • Limbic encephalitis – a “neurological” neuropsychiatric disorder
  • There is an overlap in clinical phenotype between encephalitis and schizophrenia
  • 5-9% of patients with psychoses have antibodies against a neuronal cell surface target
  • Patients with psychoses and antibodies have an abrupt onset to illness, but do not have a distinct clinical phenotype
  • Neurology and psychiatry need to combine forces!
  • The future in immunotherapy: proteins can be replaced with apitopes, representing T cell epitopes, for effective desensitization of cells causing allergy, autoimmunity and other unwanted immune responses. Apitope therapy is already proven in a range of immune pathology. Apitope immunotherapy is a targeted approach treating the underlying disease pathology by selectively reinstating immune tolerance rather than global immune suppression. (Apitope means antigen targeting epitope).

I can’t help but reinstate one of the key messages about the management of diagnosis and treatment of Autoimmune Encephalitis:

-Neurology and psychiatry need to combine forces!

A big “Thank you” and “Congratulations” to the amazing speakers and great organizers!

Your generous Donations allow IAES to continue our important work and saves lives!

Our website is not a substitute for independent professional medical advice. Nothing contained on our website is intended to be used as medical advice. No content is intended to be used to diagnose, treat, cure or prevent any disease, nor should it be used for therapeutic purposes or as a substitute for your own health professional's advice. Although THE INTERNATIONAL AUTOIMMUNE ENCEPHALITIS SOCIETY  provides a great deal of information about AUTOIMMUNE ENCEPHALITIS, all content is provided for informational purposes only. The International Autoimmune Encephalitis Society  cannot provide medical advice.

 


International Autoimmune Encephalitis Society is a charitable non-profit 501(c)(3) organization. Tax ID# 81-3752344 Donations raised directly supports patients, families and caregivers impacted by autoimmune encephalitis and to educating healthcare communities around the world.

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