Do we need to measure specific antibodies in patients with limbic encephalitis?

Abstract

Limbic encephalitis (LE) is an inflammatory brain disorder that predominantly involves the gray matter of the medial temporal lobes, resulting in mood and behavioral changes, seizures, and difficulty in forming new memories, often with retrograde memory loss.1 In most patients, the presence of an inflammatory process in the medial temporal lobes and hippocampi is visible on MRI fluid-attenuated inversion recovery (FLAIR) sequences and supported by demonstration of pleocytosis in the CSF.2–4 Nevertheless, several infections, systemic inflammatory diseases, and autoimmune mechanisms may lead to this syndrome (table). The recent descriptions of neuronal autoantibodies associated with LE have led to a dependency on antibody testing. However, many patients with autoimmune LE can be diagnosed on clinical grounds.1 This includes careful assessment of the syndrome and ancillary tests that are available in most institutions, such as routine CSF analysis with viral studies, brain MRI, and EEG, which usually shows unilateral or bilateral temporal lobe epileptic discharges or slow activity (for a review on the clinical diagnosis of LE, see reference 1). There are few infectious agents that predominantly affect the medial temporal lobes, and most of the other potential causes of LE shown in the table can be excluded after a thorough clinical history and examination. Some symptoms may even suggest the immunologic subtype of LE (e.g., faciobrachial dystonic seizures and leucine-rich glioma-inactivated 1 [LGI1] antibodies).5