Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis of suspected autoimmune origin

Pollak, Thomas A; Lennox, Belinda; Müller, Sabine; Benros, Michael E.; Prüß, Harald; Elst, Ludger Tebartz van; Klein, Hans; Steiner, Johann; Frodl, Thomas; Bogerts, Bernhard; Tian, Li; Groc, Laurent; Hasan, Alkomiet; Baune, Bernhard T.; Endres, Dominique; Haroon, Ebrahim; Yolken, Robert H.; Benedetti, Francesco; Halaris, Angelos; Meyer, Jeffrey H.; Stassen, Hans H.; Leboyer, Marion; Fuchs, Dietmar; Otto, Markus; Brown, David A.; Vincent, Angela; Najjar, Souhel; Bechter, Karl

doi:10.1016/s2215-0366(19)30290-1

Cited by 285 publications

(372 citation statements)

References 183 publications

(167 reference statements)

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“…However, the normal MRI findings, with no meningeal enhancement or brain alterations, and the response to steroid treatment support other alternative pathophysiological mechanisms. In this case, we excluded the most common causes of autoimmune encephalitis, akinetic mutism and psychosis so far [16][17][18] . All rights reserved.…”

Section: Discussionmentioning

confidence: 99%

Steroid-responsive encephalitis in Covid-19 disease

Padovani

Odolini

Masciocchi

et al. 2020

Preprint

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SARS-CoV-2 infection has the potential for targeting central nervous system and several neurological symptoms have been described in patients with severe respiratory distress. Here we described the case of an otherwise healthy 60-year old subject with SARS-CoV-2 infection but only mild respiratory abnormalities who developed severe progressive encephalopathy associated with mild pleocytosis and hyperproteinorrachia. MRI was negative whereas EEG showed theta waves on the anterior brain regions. Serum and CSF analyses excluded other known infectious or autoimmune disorders. The patient dramatically improved after high-doses steroid treatment suggesting an inflammatory-mediated brain involvement related to SARS-CoV-2 infection.

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Section: Discussionmentioning

confidence: 99%

Steroid-responsive encephalitis in Covid-19 disease

Padovani

Odolini

Masciocchi

et al. 2020

Preprint

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“…Autoimmune psychosis (AP): AP describes a syndrome with predominant psychoses and a probable autoimmune pathophysiology [21,61,67]. Initially, a distinction among the following groups was suggested: (1) psychoses with detection of classical antineuronal Abs, (2) psychoses associated with systemic inflammatory and autoimmune diseases, and (3) Ab-negative AP [61].…”

Section: Box 1: Different Nomenclature [6 22]mentioning

confidence: 99%

Autoimmune encephalitis as a differential diagnosis of schizophreniform psychosis: clinical symptomatology, pathophysiology, diagnostic approach, and therapeutic considerations

Endres

Leypoldt

Bechter

et al. 2020

Eur Arch Psychiatry Clin Neurosci

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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 newly described secondary, immune-mediated schizophreniform psychoses typically present with the acute onset of polymorphic psychotic symptoms. Over the course of the disease, other neurological phenomena, such as epileptic seizures, movement disorders, or reduced levels of consciousness, usually arise. Typical clinical signs for AEs are the acute onset of paranoid hallucinatory symptoms, atypical polymorphic presentation, psychotic episodes in the context of previous AE, and additional neurological and medical symptoms such as catatonia, seizure, dyskinesia, and autonomic instability. Predominant psychotic courses of AEs have also been described casuistically. The term autoimmune psychosis (AP) was recently suggested for these patients. Paraclinical alterations that can be observed in patients with AE/AP are inflammatory cerebrospinal fluid (CSF) pathologies, focal or generalized electroencephalographic slowing or epileptic activity, and/or suspicious "encephalitic" imaging findings. The antibody analyses in these patients include the testing of the most frequently found Abs against cell surface antigens (

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“…Thiyl radicals can also react with OH • causing the formation of very reactive sulfenic acids, which can, among others, form an intramolecular disulfide bond with cysteine and react with low-molecular thiols. Sulfenic acids are irreversibly oxidized to sulfinic acid (-SO 2 H) and sulfonic acid (SO 3 H) [10,143].…”

Section: Oxidative Nitrosative and Sulfuric Stress In Schizophreniamentioning

confidence: 99%

“…Although the trajectory of the indicated changes remains unexplained, there are reports suggesting their association with early reduction of the volume of the prefrontal cortex, superior temporal gyrus, and hippocampal gyrus volume reduction [8,9]. The probable mechanism of the observed changes in psychosis may be associated with inflammatory disorders, dysregulation of the immune system [3,10], neurodevelopmental disorders, including genetic abnormalities, i.e., 22q11.2 (22q11DS) deletion [11,12], or neutrophil functioning in the severe forms of mental disorders [10]. Their higher levels strongly correlate with positive clinical symptoms, constituting a promising marker of disease progression [13].…”

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confidence: 99%

“…McNay et al indicate that insulin signaling and abnormal glucose transport significantly affect cognitive processes and memory functions regulated by the hippocampus [265]. This is due to the incorrect activation of the insulin-sensitive GLUT4 transporter on the periphery and GLUT1-3 in the brain tissue [10]. Abnormal glucose metabolism can also affect the integrity of white and gray matter due to the effect of hyperglycemia on the dynamics and function of mitochondria, which leads to the accumulation of ROS and impaired axonal transport [266], mainly within the thalamus, parietal lobe, and hippocampus [267].…”

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confidence: 99%

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Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

et al. 2020

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Schizophrenia is a neurodevelopmental disorder featuring chronic, complex neuropsychiatric features. The etiology and pathogenesis of schizophrenia are not fully understood. Oxidative-antioxidant imbalance is a potential determinant of schizophrenia. Oxidative, nitrosative, or sulfuric damage to enzymes of glycolysis and tricarboxylic acid cycle, as well as calcium transport and ATP biosynthesis might cause impaired bioenergetics function in the brain. This could explain the initial symptoms, such as the first psychotic episode and mild cognitive impairment. Another concept of the etiopathogenesis of schizophrenia is associated with impaired glucose metabolism and insulin resistance with the activation of the mTOR mitochondrial pathway, which may contribute to impaired neuronal development. Consequently, cognitive processes requiring ATP are compromised and dysfunctions in synaptic transmission lead to neuronal death, preceding changes in key brain areas. This review summarizes the role and mutual interactions of oxidative damage and impaired glucose metabolism as key factors affecting metabolic complications in schizophrenia. These observations may be a premise for novel potential therapeutic targets that will delay not only the onset of first symptoms but also the progression of schizophrenia and its complications.

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Autoimmune psychosis: an international consensus on an approach to the diagnosis and management of psychosis of suspected autoimmune origin

Cited by 285 publications

References 183 publications

Steroid-responsive encephalitis in Covid-19 disease

Steroid-responsive encephalitis in Covid-19 disease

Autoimmune encephalitis as a differential diagnosis of schizophreniform psychosis: clinical symptomatology, pathophysiology, diagnostic approach, and therapeutic considerations

Oxidative-Antioxidant Imbalance and Impaired Glucose Metabolism in Schizophrenia

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