Onconeural Antibodies in Acute Psychiatric Inpatient Care (original) (raw)

Autoimmune Encephalitis with Antibodies: Anti-NMDAR, Anti-AMPAR, Anti-GQ1b, Anti-DPPX, Anti-CASPR2, Anti-LGI1, Anti-RI, Anti-Yo, Anti-Hu, Anti-CV2 and Anti-GABAAR, in the Course of Psychoses, Neoplastic Diseases and Paraneoplastic Syndromes

Encephalitis is a condition with a variety of etiologies, clinical presentations and degrees of severity. The causes of these disorders include both neuroinfections and autoimmune diseases in which host antibodies are pathologically directed against self antigens. In autoimmune encephalitis, autoantibodies are expressed in the central nervous system. The incidence of this disease is approximately 4% of all reported cases of encephalitis. Autoimmune encephalitis can be induced by antibodies against neuronal surface antigens such as N-methyl-D-aspartate-activated glutamate receptors (NMDAR), ⍺-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors (AMPAR) or gangliosides GQ1b, DPPX, CASPR2, LGI1, as well as by antibodies against neuronal intracellular antigens. The paper presents a number of both mental and neurological symptoms of autoimmune encephalitis. Moreover, the coexistence of psychoses, neoplastic diseases and the methods of diagnosing autoimmune encephalitis are discussed...

Anti-CNS antibodies in neurological and psychiatric disorders

Journal of Neurology, Neurosurgery & Psychiatry, 1988

TO investigate the possibility that anti-CNS antibodies may play a pathogenic role in a number of neurological and psychiatric disorders, a population study was undertaken. Serum Samples were obtained from a total of 257 adults and were screened against sodium dodecyl sulphate polyacrylamide gel electrophoretic blots of various normal, necropsy-derived adult human brain regions. The incidence of IgG immunoreactive banding in the total sample was 30%. Within the diagnostic groups the incidence of banding was: controls 32%, schizophrenia 28%, mental retardation 279'6, cerebellar ataxia 33%, Parkinson's disease 22%, myasthenia gravis 45% and epilepsy 3 1 %. The differences are not statistically significant. There was no significant difference in the numbers and locations of bands between the various diagnostic groups and the controls. The overall incidence of immunoreactivity corresponding to the high molecular weight subunit of neurofilaments was only 6%, thus not confirming a previously reported incidence of 95%. The similarity between the diagnostic and the control sera suggests that caution should be exerted in interpreting the pathogenic significance of anti-CNS immunoreactive banding on Western blots.

Autoimmune encephalitis: a potentially treatable cause of mental disorder

Advances in Psychiatric Treatment, 2014

SummaryAutoimmune encephalitides can present with altered mental states, particularly psychosis and delirium. Psychiatrists need to be particularly vigilant in cases of first-episode psychosis and to look out for other, sometimes subtle, features of encephalitis. Encephalitis related to N-methyl-d-aspartate (NMDA) receptor autoantibodies is the most common autoimmune cause of isolated psychosis, the second being related to voltage-gated potassium channel (VGKC)-complex antibodies. Psychiatrists should note ‘red flag’ signs of seizures, autonomic instability, movement disorders and sensitivity to antipsychotic medication (including neuroleptic malignant syndrome). They should also be aware that, in some cases, encephalitis is a non-metastatic manifestation of malignancy. Treatment primarily involves suppression of immunity and is often successful if delivered early. There is accumulating evidence that isolated psychiatric syndromes can be caused by autoimmunity and this could potenti...

Autoimmune encephalitis in psychiatric institutions: current perspectives

Neuropsychiatric disease and treatment, 2016

Autoimmune encephalitis is a rare and newly described group of diseases involving autoantibodies directed against synaptic and neuronal cell surface antigens. It comprises a wide range of neuropsychiatric symptoms. Sensitive and specific diagnostic tests such as cell-based assay are primordial for the detection of neuronal cell surface antibodies in patients' cerebrospinal fluid or serum and determine the treatment and follow-up of the patients. As neurological symptoms are fairly well described in the literature, this review focuses on the nature of psychiatric symptoms occurring at the onset or during the course of the diseases. In order to help the diagnosis, the main neurological symptoms of the most representative synaptic and neuronal cell surface autoantibodies were detailed. Finally, the exploration of these autoantibodies for almost a decade allowed us to present an overview of autoimmune encephalitis incidence in psychiatric disease and the general guidelines for the m...

Routine diagnostics for neural antibodies, clinical correlates, treatment and functional outcome

Journal of Neurology, 2020

Objective To determine frequencies, interlaboratory reproducibility, clinical ratings, and prognostic implications of neural antibodies in a routine laboratory setting in patients with suspected neuropsychiatric autoimmune conditions. Methods Earliest available samples from 10,919 patients were tested for a broad panel of neural antibodies. Sera that reacted with leucine-rich glioma-inactivated protein 1 (LGI1), contactin-associated protein-2 (CASPR2), or the voltage-gated potassium channel (VGKC) complex were retested for LGI1 and CASPR2 antibodies by another laboratory. Physicians in charge of patients with positive antibody results retrospectively reported on clinical, treatment, and outcome parameters. Results Positive results were obtained for 576 patients (5.3%). Median disease duration was 6 months (interquartile range 0.6–46 months). In most patients, antibodies were detected both in CSF and serum. However, in 16 (28%) patients with N-methyl-d-aspartate receptor (NMDAR) anti...

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

European Archives of Psychiatry and Clinical Neuroscience, 2020

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 (

122. High Antigliadin Antibodies (IgG) are Linked to Peripheral and Central Measures of Inflammation in a Subset of People With Schizophrenia

Schizophrenia Bulletin

Background: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is one of autoimmune limbic encephalitis which receives the most attention in the psychiatric field. Patients with anti-NMDAR encephalitis typically exhibit psychiatric symptoms such as hallucination, delusion, aggression, manic episodes, and abnormal behaviors. With the given psychiatric symptoms, those patients are often diagnosed as atypical psychosis or schizophrenia and medicated with antipsychotic drugs. The definite diagnosis of anti-NMDAR encephalitis still remains to be established, however. Methods: The subjects were the patients whose cerebrospinal fluids (CSF) were verified to contain anti-NMDAR1 receptor (GRIN1) auto-antibodies and thus were diagnosed as anti-NMDAR encephalitis. These subjects exhibited chronic or subacute symptoms which were classified into typical psychosis (21 patients) and atypical psychosis (20 patients). We measured the immunoreactivity for NMDAR1 in the cell-based immunoassay in all CSF samples as well as in some of their serum samples (37 patients). This study was approved by the authorization of the Kanazawa Medical College Ethics Committee and Niigata University Medical Ethics Committee. All the patients provided written informed consent to allow the use of CSF and blood samples for this investigation. Results: Although all the CSF samples were positive for the auto-antibodies, the positive frequency of their blood samples was lower in the subjects with atypical psychosis (23.5%; 4 patients) than in those with typical psychosis (65.0%; 13 patients) (P < .05). In addition, the auto-antibody titres were significantly lower in both CSF (P < .05) and serum (P < .01) of the subjects with atypical psychosis. Conclusion: These results suggest that the patients with anti-NMDAR encephalitis, but not with typical psychotic symptoms, often exhibit lower or undetectable blood concentrations of anti-NMDAR1 auto-antibodies. Thus, the definite diagnosis of anti-NMDAR encephalitis requires CSF examination.

Autoimmunity in Neurological and Psychiatric Disorders: Participation of Antibodies and Cytokines in the Immunopathogenesis of these Diseases

2014

Angel Alberto Justiz Vaillant1*, Wayne Mohammed1, Sehlule Vuma1 and Norma Anderson2 1Department of Para-clinical Sciences, Faculty of Medical Sciences, The University of the West Indies, St. Augustine Campus, Trinidad and Tobago, West Indies 2Department of Basic Medical Sciences, The University of the West Indies, Mona campus, Jamaica, West Indies *Corresponding author: Angel Alberto Justiz Vaillant, Department of Para-clinical Sciences, Faculty of Medical Sciences, The University of the West Indies, St. Augustine Campus, Trinidad and Tobago, West Indies, E-mail: avail4883@gmail.com