2020
DOI: 10.1007/s00406-020-01113-2
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Autoimmune encephalitis as a differential diagnosis of schizophreniform psychosis: clinical symptomatology, pathophysiology, diagnostic approach, and therapeutic considerations

Abstract: Primary schizophreniform psychoses are thought to be caused by complex gene-environment interactions. Secondary forms are based on a clearly identifiable organic cause, in terms of either an etiological or a relevant pathogenetic factor. The secondary or "symptomatic" forms of psychosis have reentered the focus stimulated by the discovery of autoantibody (Ab)associated autoimmune encephalitides (AEs), such as anti-NMDA-R encephalitis, which can at least initially mimic variants of primary psychosis. These newl… Show more

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Cited by 70 publications
(66 citation statements)
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“…Secondary forms of movement disorders may occur in the context of autoimmune encephalitis with different antineuronal antibodies [ 12 , 13 , 14 , 15 ]. Dyskinesias are found in anti-NMDA-receptor (R) encephalitis.…”
Section: Introductionmentioning
confidence: 99%
“…Secondary forms of movement disorders may occur in the context of autoimmune encephalitis with different antineuronal antibodies [ 12 , 13 , 14 , 15 ]. Dyskinesias are found in anti-NMDA-receptor (R) encephalitis.…”
Section: Introductionmentioning
confidence: 99%
“…▶ Tab. 3 Spezifische Empfehlungen zur organischen Diagnostik bei immunologischen Psychosen (gemäß [7][8][9]). [11,16].…”
Section: Pr a Xistippunclassified
“…Zu den Zweitlinienverfahren gehören Rituximab und Cyclophosphamid, wobei Rituximab zunehmend wichtiger wird [9,[11][12][13][14][15]. Während ein Therapieversuch mit Kortison dabei auch im klassischen Setting der Psychiatrie meist gut umgesetzt werden kann, muss bei weiterer Therapieeskalation die Zusammenarbeit mit der Neurologie, Immunologie und Nephrologie gesucht werden.…”
Section: Therapeutische Implikationenunclassified
See 1 more Smart Citation
“…Autoimmune encephalitis, such as anti-NMDA-receptor encephalitis, is typically associated with a subacute onset of neuropsychiatric symptoms, and can often be identified by the presence of antineuronal autoantibodies or inflammatory changes in the cerebrospinal fluid (CSF), electroencephalography (EEG) pathologies, and evidence of encephalitis in magnetic resonance imaging (MRI) or [18F]fluorodeoxyglucose positron emission tomography (FDG PET; [1][2][3][4][5]. Until now, a series of antineuronal autoantibodies against surface (e.g., NMDA-R, LGI1, CASPR2, AMPA1/2-R, GABA-B-R, DPPX) or intracellular antigens (e.g., Yo, Hu, CV2/CRMP5, Ri, Ma1/2, SOX1, GAD65, amphiphysin), or "potentially antineuronal" systemic antibodies (e.g., antinuclear antibodies [ANAs] against double-stranded [ds]-DNA or gliadin autoantibodies) (3)(4)(5) are known. The associated neuropsychiatric syndromes are classically characterized by a combination of neurological (e.g., seizures, movement disorders, focalneurological deficits, or reduced consciousness) and psychiatric (e.g., psychosis, mania, or catatonia) symptoms (3,6,7).…”
Section: Introductionmentioning
confidence: 99%