"In those select cases with this severity of symptoms, ECT has been shown to be successful. Previous reports have shown that seven to eight bilateral ECT treatments over 2–4 weeks have provided symptom remission in catatonia associated with anti-NMDA-R encephalitis.5,48,49 For the minority of patients with worsening movement disorders and level of consciousness who fail to respond to first-line therapy, ECT should be considered as an adjunct treatment. "
[Show abstract][Hide abstract] ABSTRACT: Objective
Anti-N-methyl-D-aspartate-receptor (NMDA-R) encephalitis is a new autoimmune disorder, often paraneoplastic in nature, presenting with complex neuropsychiatric symptoms. Diagnosed serologically, this disorder is often responsive to immunosuppressant treatment. The objective of this review is to educate clinicians on the challenges of diagnosis and management of this disorder.
Materials and methods
A review of the relevant literature on clinical presentation, pathophysiology, and recommended management was conducted using a PubMed search. Examination of the results identified articles published between 2007 and 2014.
The literature highlights the importance of recognizing early common signs and symptoms, which include hallucinations, seizures, altered mental status, and movement disorders, often in the absence of fever. Although the presence of blood and/or cerebrospinal fluid autoantibodies confirms diagnosis, approximately 15% of patients have only positive cerebrospinal fluid titers. Antibody detection should prompt a search for an underlying teratoma or other underlying neoplasm and the initiation of first-line immunosuppressant therapy: intravenous methylprednisolone, intravenous immunoglobulin, or plasmapheresis, or a combination thereof. Second-line treatment with rituximab or cyclophosphamide should be implemented if no improvement is noted after 10 days. Complications can include behavioral problems (eg, aggression and insomnia), hypoventilation, catatonia, and autonomic instability. Those patients who can be managed outside an intensive care unit and whose tumors are identified and removed typically have better rates of remission and functional outcomes.
There is an increasing need for clinicians of different specialties, including psychiatrists, neurologists, oncologists, neurooncologists, immunologists, and intensivists to become familiar with this disorder and its potential complications. Remission can be optimized with prompt detection and aggressive, collaborative treatment within a multidisciplinary team.
"It has now been suggested that the NMDAR antibody interferes with glutamatergic signalling by selectively decreasing the number of NMDAR clusters in the postsynaptic density.161) In fact, prominent psychiatric symptoms such as psychosis, catatonia-like symptoms and dyskinesias in patients with encephalitis162,163) can be triggered by IgG serum and CSF antibodies that are directed against extracellular epitopes of the NR1a subunit of NMDARs.164) Recent studies found that approximately 5-10% of SCZ cases were associated with serum and CSF autoantibodies to the NMDAR.165-167) "
[Show abstract][Hide abstract] ABSTRACT: Schizophrenia (SCZ) is a polygenic, multi-factorial disorder and a definitive understanding of its pathophysiology has been lacking since it was first described more than a century ago. The predominant pharmacological approach used to treat SCZ is the use of dopamine receptor antagonists. The fact that many patients remain symptomatic, despite complying with medication regimens, emphasises the need for a more encompassing explanation for both the causes and treatment of SCZ. Recent neuroanatomical, neurobiological, environmental and genetic studies have revived the idea that inflammatory pathways are involved in the pathogenesis of SCZ. These new insights have emerged from multiple lines of evidence, including the levels of inflammatory proteins in the central nervous system of patients with SCZ and animal models. This review focuses on aberrant inflammatory mechanisms present both before and during the onset of the psychotic symptoms that characterise SCZ and discusses recent research into adjunctive immune system modulating therapies for its more effective treatment.
Clinical Psychopharmacology and Neuroscience 12/2013; 11(3):107-117. DOI:10.9758/cpn.2013.11.3.107
"In the last few years, a number of antibodies to neuronal cell surface antigens have been identified in cases of autoimmune encephalitis that respond to immunotherapy [29,30]. Over two-thirds of patients with NMDAR antibody encephalitis have prominent psychiatric symptoms or may present to psychiatric services in the first instance [23,29,31-33]. The psychiatric symptoms are those seen in schizophrenia including delusions, hallucinations, and catatonic movement disorder. "
[Show abstract][Hide abstract] ABSTRACT: Causative role of encephalitis in major psychotic features, dyskinesias (particularly orofacial), seizures, and autonomic and respiratory changes has been recently emphasized. These symptoms often occur in young females with ovarian teratomas and are frequently associated with serum and CSF autoantibodies to the NMDA receptor (NMDAR).
The study included a total of 61 patients from age 15 to 61 and was carried out between January 1, 2005, and Dec 31, 2010. The patients were divided into the following three clinical groups for comparison. Group A; Patients with typical clinical characteristics of anti-NMDAR encephalitis. Group B; Patients with narcolepsy with severe psychosis. Group C; Patients with schizophrenia or schizo-affective disorders.
Ten out of 61 cases were anti-NMDAR antibody positive in typical encephalitis cases (group A: 3 of 5 cases) and cases in a broader range of psychiatric disorders including narcolepsy (group B: 3 of 5 cases) and schizophrenia (group C: 4 of 51 cases).
In addition to 3 typical cases, we found 7 cases with anti-NMDAR antibody associated with various psychotic and sleep symptoms, which lack any noticeable clinical signs of encephalitis (seizures and autonomic symptoms) throughout the course of the disease episodes; this result suggest that further discussion on the nosology and pathophysiology of autoimmune-mediated atypical psychosis and sleep disorders is required.
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