scholarly journals Autoimmune Encephalitis Associated with Anti-gamma-aminobutyric Acid B Receptor Antibodies Mimicking Syncope

2020 ◽  
Vol 59 (6) ◽  
pp. 843-847 ◽  
Author(s):  
Yuki Kitazaki ◽  
Masamichi Ikawa ◽  
Tomohisa Yamaguchi ◽  
Soichi Enomoto ◽  
Toru Kishitani ◽  
...  
Keyword(s):  
Autoimmune Encephalitis ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Receptor Antibodies

scholarly journals Positive Anti-GABAB Receptor Antibodies in a Patient with Hashimoto’s Thyroiditis and Bipolar Affective Disorder

2021 ◽  
pp. 1-3
Author(s):  
Polina A. Sobolevskaia ◽  
Boris V. Andreev ◽  
Leonid P. Churilov ◽  
Tamara V. Fedotkina ◽  
Boris Gilburd ◽  
...  
Keyword(s):  
Affective Disorder ◽  
Gabab Receptor ◽  
Bipolar Affective Disorder ◽  
Autoimmune Encephalitis ◽  
Thyroid Peroxidase ◽  
Gamma Aminobutyric Acid ◽  
Brain Disorder ◽  
Acid Type ◽  
Nosological Entity ◽  
Receptor Antibodies

A kind of autoimmune encephalitis with positive autoantibodies toward the B1 subunit of the gamma-aminobutyric acid-type B receptor is known as anti-GABABR encephalitis. It is an autoimmune brain disorder with typical manifestations of a limbic encephalitis. It can coexist with positive anti-thyroid autoantibodies. We described a 57-year-old woman who was diagnosed with a bipolar affective disorder. The patient had high titers of anti-thyroid peroxidase antibodies, and she also was positive for anti-GABABR antibodies. There is a question, if this case is a kind of comorbidity of anti-thyroid and anti-brain autoimmunity or is it a single nosological entity – a kind of Hashimoto’s encephalopathy?

scholarly journals Evaluation of seizure treatment in anti-LGI1, anti-NMDAR, and anti-GABABR encephalitis

Neurology ◽  
2019 ◽  
Vol 92 (19) ◽  
pp. e2185-e2196 ◽  
Author(s):  
Marienke A.A.M. de Bruijn ◽  
Agnes van Sonderen ◽  
Marleen H. van Coevorden-Hameete ◽  
Anna E.M. Bastiaansen ◽  
Marco W.J. Schreurs ◽  
...  
Keyword(s):  
Side Effects ◽  
Medical Information ◽  
Autoimmune Encephalitis ◽  
Epileptic Seizures ◽  
Aminobutyric Acid ◽  
Seizure Freedom ◽  
Disease Course ◽  
Gamma Aminobutyric Acid ◽  
Psychotic Behavior ◽  
New Onset

ObjectiveThis nationwide cohort study evaluates seizure responses to immunotherapy and antiepileptic drugs (AEDs) in patients with anti-leucine-rich glioma-inactivated 1 (LGI1), anti-NMDA receptor (NMDAR), and anti-gamma-aminobutyric-acid B receptor (GABABR) encephalitis.MethodsAnti-LGI1, anti-NMDAR, and anti-GABABR encephalitis patients with new-onset seizures were included. Medical information about disease course, AEDs and immunotherapies used, effects, and side effects were collected. Outcome measures were (1) seizure freedom while using AEDs or immunotherapy, (2) days to seizure freedom from start of AEDs or immunotherapy, and (3) side effects.ResultsOf 153 patients with autoimmune encephalitis (AIE) (53 LGI1, 75 NMDAR, 25 GABABR), 72% (n = 110) had epileptic seizures, and 89% reached seizure freedom. At least 53% achieved seizure freedom shortly after immunotherapy, and 14% achieved seizure freedom while using only AEDs (p < 0.0001). This effect was similar in all types (p = 0.0001; p = 0.0005; p = 0.013, respectively). Median time to seizure freedom from AEDs start was 59 days (interquartile range [IQR] 27–160), and 28 days from start of immunotherapy (IQR 9–71, p < 0.0001). Side effects were psychotic behavior and suicidal thoughts by the use of levetiracetam, and rash by the use of carbamazepine. Carbamazepine was more effective than levetiracetam in reducing seizures in anti-LGI1 encephalitis (p = 0.031). Only 1 patient, of 86 surviving patients, developed epilepsy after resolved encephalitis.ConclusionEpilepsy after resolved encephalitis was rare in our cohort of patients with AIE treated with immunotherapy. In addition, seizure freedom is achieved faster and more frequently after immunotherapy. Therefore, AEDs should be considered as add-on treatment, and similar to treatment of other encephalitis symptoms, immunotherapy is crucial.

scholarly journals Rituximab for Autoimmune Encephalitis with Epilepsy

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Mohankumar Kurukumbi ◽  
Rahul H. Dave ◽  
Jose Castillo ◽  
Tulsi Shah ◽  
Joanne Lau
Keyword(s):  
Intractable Epilepsy ◽  
Autoimmune Encephalitis ◽  
Aminobutyric Acid ◽  
High Dose ◽  
Gamma Aminobutyric Acid ◽  
Acid Receptor ◽  
Voltage Gated ◽  
Aspartate Receptor ◽  
A Cell

Intractable epilepsy remains a significant medical challenge, resulting in recurrent and prolonged intensive care unit (ICU) admissions. Autoimmune encephalitis is emerging as a treatable cause of intractable epilepsy. It is characterized by antibodies against cerebral antigens, such as potassium channels such as leucine-rich, glioma inactivated 1 (LGI1) and contactin-associated protein 2 (CASPR2), calcium channels such as the voltage-gated calcium channel (VGCC), or neurotransmitter receptors such as the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), gamma aminobutyric acid receptor (GABAR), and N-methyl-D-aspartate receptor (NMDAR). Diagnosis requires a syndrome consistent with an antibody identified in serum or cerebrospinal fluid (CSF) using methods that minimize risk of false-positives. Although there is no officially approved therapy for these disorders, typical approaches involve chronic high-dose steroids, intravenous immunoglobulin (IVIG), or plasma exchange. Rituximab is effective for antibody-associated disorders such as lupus, myasthenia gravis, and neuromyelitis optica. Here, we present three patients who were admitted with recalcitrant status epilepticus and demonstrated serum antibodies against NMDAR, LGI1, or VGCC using a cell-based assay. All patients demonstrated complete, long-term epilepsy control and improvement in symptoms with rituximab.

Catatonia with GABAA receptor antibodies

2019 ◽  
Vol 20 (2) ◽  
pp. 139-143 ◽  
Author(s):  
Kiran Samra ◽  
Jonathan Rogers ◽  
Mohamed Mahdi-Rogers ◽  
Biba Stanton
Keyword(s):  
Behavioural Change ◽  
Autoimmune Encephalitis ◽  
African Woman ◽  
Causative Role ◽  
Gamma Aminobutyric Acid ◽  
Antibody Treatment ◽  
Gradual Improvement ◽  
Sharp Waves ◽  
Oral Corticosteroids ◽  
Receptor Antibodies

A 22-year-old African woman developed acute behavioural change, against a background of sickle cell disease with strokes requiring a ventriculoperitoneal shunt. She alternated between mutism with prolonged staring and posturing, and a state of agitation with elation and echolalia. Cerebrospinal fluid (CSF) protein was elevated and electroencephalogram showed mild slowing with bitemporal slow and sharp waves. We suspected catatonia secondary to possible autoimmune encephalitis but her condition persisted despite intravenous methylprednisolone. After identifying a positive serum anti-gamma-aminobutyric acid-A (GABAA) antibody, treatment with intravenous immunoglobulin, oral corticosteroids and rituximab led to gradual improvement. Patients with catatonia may show reduced GABAA receptor density and there are two other reports of catatonia with anti-GABAA antibodies. This patient’s treatment response supports the antibody’s causative role.

Purification of Antihemophilic Factor (Factor VIII) by Amino Acid Precipitation*

1964 ◽  
Vol 11 (01) ◽  
pp. 064-074 ◽  
Author(s):  
Robert H Wagner ◽  
William D McLester ◽  
Marion Smith ◽  
K. M Brinkhous
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Factor Viii ◽  
Plasma Protein ◽  
Acid Precipitation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Specific Procedure ◽  
Beta Alanine ◽  
Antihemophilic Factor

Summary1. The use of several amino acids, glycine, alpha-aminobutyric acid, alanine, beta-alanine, and gamma-aminobutyric acid, as plasma protein precipitants is described.2. A specific procedure is detailed for the preparation of canine antihemophilic factor (AHF, Factor VIII) in which glycine, beta-alanine, and gammaaminobutyric acid serve as the protein precipitants.3. Preliminary results are reported for the precipitation of bovine and human AHF with amino acids.

A Simple Method for Preparing Fibrinogen

1966 ◽  
Vol 16 (01/02) ◽  
pp. 198-206 ◽  
Author(s):  
W Straughn ◽  
R. H Wagner
Keyword(s):  
Barium Sulfate ◽  
Caproic Acid ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Human Fibrinogen ◽  
Simple Method ◽  
High Yields ◽  
Marked Stability

SummaryA simple new procedure is reported for the isolation of canine, bovine, porcine, and human fibrinogen. Two molar β-alanine is used to precipitate fibrinogen from barium sulfate adsorbed plasma. The procedure is characterized by dependability and high yields. The material is 95% to 98% clottable protein but still contains impurities such as plasminogen and fibrin-stabilizing factor. Plasminogen may be removed by adsorption with charcoal. The fibrinogen preparations exhibit marked stability to freezing, lyophilization, and dialysis. Epsilon-amino-n-caproic acid and gamma-aminobutyric acid which were also studied have the property of precipitating proteins from plasma but lack the specificity for fibrinogen found with β-alanine.

Understanding Schizophrenia: Genetic Causes and Treatment

2019 ◽  
Vol 1 (1) ◽  
pp. 6-12
Author(s):  
Fatima Javeria ◽  
Shazma Altaf ◽  
Alishah Zair ◽  
Rana Khalid Iqbal
Keyword(s):  
Copy Number ◽  
Drug Targets ◽  
Disease Risk ◽  
Mental Disease ◽  
Copy Number Variants ◽  
Aminobutyric Acid ◽  
Epigenetic Mechanisms ◽  
Gamma Aminobutyric Acid ◽  
Wide Range ◽  
Severe Mental Disease

Schizophrenia is a severe mental disease. The word schizophrenia literally means split mind. There are three major categories of symptoms which include positive, negative and cognitive symptoms. The disease is characterized by symptoms of hallucination, delusions, disorganized thinking and speech. Schizophrenia is related to many other mental and psychological problems like suicide, depression, hallucinations. Including these, it is also a problem for the patient’s family and the caregiver. There is no clear reason for the disease, but with the advances in molecular genetics; certain epigenetic mechanisms are involved in the pathophysiology of the disease. Epigenetic mechanisms that are mainly involved are the DNA methylation, copy number variants. With the advent of GWAS, a wide range of SNPs is found linked with the etiology of schizophrenia. These SNPs serve as ‘hubs’; because these all are integrating with each other in causing of schizophrenia risk. Until recently, there is no treatment available to cure the disease; but anti-psychotics can reduce the disease risk by minimizing its symptoms. Dopamine, serotonin, gamma-aminobutyric acid, are the neurotransmitters which serve as drug targets in the treatment of schizophrenia. Due to the involvement of genetic and epigenetic mechanisms, drugs available are already targeting certain genes involved in the etiology of the disease.

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