Autoimmune limbic encephalitis (Q84129): Difference between revisions
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A encefalite límbica autoimune é uma doença imunomediada do sistema límbico ou dos lobos temporais mediais. A base de tal autoimunidade permanece obscura em muitos casos, mas pode ocorrer após uma variedade de infecções virais. Ao contrário da encefalite paraneoplásica, um tumor não está presente. Normalmente se manifesta com declínio cognitivo rapidamente progressivo, frequentemente com convulsões associadas, embora o tronco cerebral e os núcleos da base possam ocorrer. Os pacientes também podem se queixar de cefaleia, irritabilidade, distúrbios do sono, delírios, alucinações, agitação e psicose. Os sintomas neurológicos podem responder favoravelmente à imunoterapia. As investigações podem revelar anormalidades do sinal T2 do lobo temporal mesial na ressonância magnética e um líquido cefalorraquiano inflamatório._x000D_ _x000D_ Os autoanticorpos neurais associados incluem: anticorpos neurais direcionados a antígenos da membrana plasmática, eles são efetores de lesão (por exemplo, anticorpos de canal de potássio controlado por voltagem - subtipos LGI1 ou CASPR2). | |||
| description / en | description / en | ||
Autoimmune limbic encephalitis is an immune mediated disease of the limbic system or medial temporal lobes. The basis of such autoimmunity remains unclear in many cases but may follow a variety of viral infections. Unlike paraneoplastic encephalitis, a tumour is not present. It typically manifests with rapidly progressive cognitive decline often with accompanying seizures although brainstem and basal ganglia involvement may occur. Patients may also complain of headache, irritability, sleep disturbance, delusions, hallucinations, agitation, and psychosis. Neurological symptoms may respond favourably to immunotherapy. Investigations may reveal mesial temporal lobe T2 signal abnormalities on MRI and an inflammatory spinal fluid. Associated neural autoantibodies include: neural antibodies targeting plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel antibodies-LGI1 or CASPR2 subtypes). | |||
Revision as of 09:29, 15 August 2026
Autoimmune limbic encephalitis is an immune mediated disease of the limbic system or medial temporal lobes. The basis of such autoimmunity remains unclear in many cases but may follow a variety of viral infections. Unlike paraneoplastic encephalitis, a tumour is not present. It typically manifests with rapidly progressive cognitive decline often with accompanying seizures although brainstem and basal ganglia involvement may occur. Patients may also complain of headache, irritability, sleep disturbance, delusions, hallucinations, agitation, and psychosis. Neurological symptoms may respond favourably to immunotherapy. Investigations may reveal mesial temporal lobe T2 signal abnormalities on MRI and an inflammatory spinal fluid. Associated neural autoantibodies include: neural antibodies targeting plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel antibodies-LGI1 or CASPR2 subtypes).
| Language | Label | Description | Also known as |
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| default for all languages | ID_1254443511 |
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| English | Autoimmune limbic encephalitis |
Autoimmune limbic encephalitis is an immune mediated disease of the limbic system or medial temporal lobes. The basis of such autoimmunity remains unclear in many cases but may follow a variety of viral infections. Unlike paraneoplastic encephalitis, a tumour is not present. It typically manifests with rapidly progressive cognitive decline often with accompanying seizures although brainstem and basal ganglia involvement may occur. Patients may also complain of headache, irritability, sleep disturbance, delusions, hallucinations, agitation, and psychosis. Neurological symptoms may respond favourably to immunotherapy. Investigations may reveal mesial temporal lobe T2 signal abnormalities on MRI and an inflammatory spinal fluid. Associated neural autoantibodies include: neural antibodies targeting plasma membrane antigens they are effectors of injury (e.g. voltage gated potassium channel antibodies-LGI1 or CASPR2 subtypes). |
