Neuropsychiatric Disorders Due to Limbic Encephalitis: Immunologic Aspect

Abstract

Limbic encephalitis (LE) is a rare cause of encephalitis presenting as an acute and subacute onset of neuropsychiatric manifestations, particularly with memory deficits and confusion as core features, along with seizure occurrence, movement disorders, or autonomic dysfunctions. LE is caused by neuronal antibodies targeting the cellular surface, synaptic, and intracellular antigens, which alter the synaptic transmission, especially in the limbic area. Immunologic mechanisms involve antibodies, complements, or T-cell-mediated immune responses in different degree according to different autoantibodies. Sensitive cerebrospinal fluid markers of LE are unavailable, and radiographic findings may not reveal a typical mesiotemporal involvement at neurologic presentations; therefore, a high clinical index of suspicions is pivotal, and a neuronal antibody testing is necessary to make early diagnosis. Some patients have concomitant tumors, causing paraneoplastic LE; therefore, tumor survey and treatment are required in addition to immunotherapy. In this study, a review on the molecular and immunologic aspects of LE was conducted to gain awareness of its peculiarity, which we found quite different from our knowledge on traditional psychiatric illness.

FDG-PET-Bildgebung der limbischen Enzephalitis

“…Hervorragende Zusammenfassungen des Kenntnisstands zu Art, Häufigkeit, Pathomechanismen und Therapie von Autoimmunenzephalitiden finden sich in [15,29]. Anwendungsorientierte Zusammenfassungen für den Kliniker finden sich in [2, 14,30,31,32,33], für Autoimmunenzephalitiden speziell bei älteren Patienten in [34,35].…”

Autoimmune Limbic Encephalitis: A Review of Clinicoradiological Features and the Challenges of Diagnosis

“…Local pathologic effects following antibody-antigen interaction include direct blockade of cell-surface channels and receptors and internalization of cell-surface receptors. The autoantibodies may also activate natural killer cells or the complement system and thus promote complement-mediated or cell-mediated cytotoxicity and subsequent neuronal death [ 16 ].…”

Neuropsychological implication in possible antibody-negative limbic encephalitis: a clinical case report

“…3,4 Other antibodies include anti-a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor antibodies, anti-gammaaminobutyric-acid B receptor antibodies and antibodies to other antigens present in the neuropil of the hippocampus and cerebellum. 5 However, previous studies reported that some patients presented with LE antibody-negative. 6,7 Limbic encephalitis includes a broad spectrum of clinical symptoms with subacute onset and it can cause persistent brain damage.…”