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paraneoplastic limbic encephalitis

Etiology: 1) mediators: a) intracellular autoantigens: - anti-Hu, CV2/CRMP5 b) cell-surface autoantigens - CASPR2 (LG1), formerly thought to be VGKC - NMDA receptor - LBI1 protein 2) associated neoplasms: a) small cell lung cancer b) thymoma c) ovarian teratoma, testicular teratoma d) breast cancer [3] e) Hodgkin's lymphoma Epidemiology: rare Pathology: 1) neuronal loss in medial temporal lobe & elsewhere in the limbic system 2) perivascular & meningeal lymphocytic infiltration Clinical manifestations: 1) evolution over weeks to months* - patients frequently present with neurologic symptoms prior to diagnosis of malignancy - acute or subacute mood & behavioral changes 2) agitation 3) confusional state 4) memory loss with progession to dementia 5) seizures [2] 6) personality change 7) psychosis 8) oral dyskinesias 9) SIADH (lung cancer, thymoma) * distinguishing from Herpes simplex encephalitis Laboratory: - anti-NMDA receptor antibody - anti-AMPA receptor antibody - anti-CASPR2 - contactin-associated protein 2 IgG in CSF - contactin-associated protein 2 IgG in serum/plasma - anti-Hu - anti-CRMP5 - anti-GABA B receptor - GABBR Ab in serum - GABBR IgG in serum - GABBR IgG in CSF - voltage-gated potassium channel Ab in CSF [3] - LG1 Ab in CSF [3] - LGI1 Ab in CSF [3] - CSF analysis may show lymphocytic pleocytosis Special laboratory: - EEG may be abnormal Radiology: - MRI may be abnormal Differential diagnosis: - Herpes simplex encephalitis evolves over days [3] - anti-NMDA receptor encephalitis - anti-leucine-rich glioma inactivated 1 encephalitis Management: 1) treat empirically with intravenous acyclovir for Herpes simplex encephalitis until diagnosis is clarified [3] 2) intracellular autoantigen (+) - generally refractory to therapy 3) cell-surface autoantigen (+) a) removal of tumor b) glucocorticoids c) IV gamma-globulin d) plasmapheresis 4) evaluation/surveillance for systemic neoplasm may need to continue for years after initial presentation

Interactions

disease interactions

Related

anti-Hu antibody (type-1 ANNA) hippocampal 38K autoantigen

Specific

anti-leucine-rich glioma inactivated 1 (LGI1) encephalitis anti-NMDA receptor encephalitis; NMDAR Ab encephalitis

General

limbic encephalitis paraneoplastic neurologic syndrome

References

  1. Harrison's Principles of Internal Medicine, 14th ed. Fauci et al (eds), McGraw-Hill Inc. NY, 1998, pg 624
  2. Tuzun E & Dalmau J Limbic encephalitis and variants: Classification, diagnosis and treatment. Neurologist 2007, 13:261 PMID: 17848866
  3. Medical Knowledge Self Assessment Program (MKSAP) 16, 17, 19 American College of Physicians, Philadelphia 2012, 2015, 2021