Abstract
Limbic encephalitis is characterized by adaptive autoimmune inflammation of the gray matter structures of the limbic system. It has recently been identified as a major cause of temporal lobe epilepsy accompanied by progressive declarative – mainly episodic – memory disturbance as well as a variety of rather poorly defined emotional and behavioral changes. While autoimmune inflammation of the hippocampus is likely to be responsible for declarative memory disturbance, consequences of autoimmune inflammation of the amygdala are largely unknown. The amygdala is central for the generation of adequate homoeostatic behavioral responses to emotionally significant external stimuli following processing in a variety of parallel neuronal circuits. Here, we hypothesize that adaptive cellular and humoral autoimmunity may target and modulate distinct inhibitory or excitatory neuronal networks within the amygdala, and thereby strongly impact processing of emotional stimuli and corresponding behavioral responses. This may explain some of the rather poorly understood neuropsychiatric symptoms in limbic encephalitis.
Highlights
We hypothesize that adaptive cellular and humoral autoimmunity may target and modulate distinct inhibitory or excitatory neuronal networks within the amygdala, and thereby strongly impact processing of emotional stimuli and corresponding behavioral responses
Limbic encephalitis is characterized by adaptive autoimmune inflammation of the gray matter structures of the limbic system
It has recently been identified as a major cause of temporal lobe epilepsy accompanied by progressive declarative – mainly episodic – memory disturbance as well as a variety of rather poorly defined emotional and behavioral changes
Summary
We hypothesize that adaptive cellular and humoral autoimmunity may target and modulate distinct inhibitory or excitatory neuronal networks within the amygdala, and thereby strongly impact processing of emotional stimuli and corresponding behavioral responses. Considering these findings, we hypothesize that changes in BLA excitability and information processing induced by autoimmune inflammation contribute to seizures, different levels of anxiety, mood disorder, and potentially memory deficits in limbic encephalitis as – depending on the predominant immune effector mechanism and the neuronal target antigen – autoimmune inflammation of the amygdala may result in decreased or increased excitability and function of principal neurons of the BLA network (Figure 1; Table 1).
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