ReviewFrontiers in immunology2022
Catatonic Schizophrenia Associated With Cerebrospinal GAD65 Autoantibodies: Case Report and Literature Review.
Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular Mimicry BetweenInternational journal of molecular sciences · 2025Article
- The Role of GABA Pathway Components in Pathogenesis of Neurodevelopmental Disorders.International journal of molecular sciences · 2025Review
- Neuronal autoantibodies in the cerebrospinal fluid of 148 patients with schizophrenia and 151 healthy controls.Heliyon · 2024Article
- Multiple serum anti-glutamate receptor antibody levels in clozapine-treated/naïve patients with treatment-resistant schizophrenia.BMC psychiatry · 2024Article
- Orexin/hypocretin system dysfunction in patients with Takotsubo syndrome: A novel pathophysiological explanation.Frontiers in cardiovascular medicine · 2022Article
- Orexin/Hypocretin System Dysfunction in ESSENCE (Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations).Neuropsychiatric disease and treatment · 2022Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: GAD65 autoimmunity is reported to be associated with schizophrenia and bipolar disorder. However, there has been no evidence that glutamic acid decarboxylase 65 (GAD65) autoantibodies in cerebrospinal fluid (CSF) are associated with akinetic catatonia in schizophrenia patients. Methods: We report the case of a 28-year-old man who underwent diagnostics including brain MRI, neuropsychological testing, and electroencephalography (EEG) as well as a tumor search Results: Our patient presented catatonia that responded somewhat to benzodiazepines in combination with previously taken antipsychotics such as risperidone for prediagnosed paranoid schizophrenia. Diagnostics revealed GAD65 autoantibodies in his serum and CSF. MRI revealed no brain lesion, and the tumor search had no malignancy. We diagnosed catatonic schizophrenia. Furthermore, as he had not fully recovered, he was given immunotherapy entailing two cycles of intravenous immunoglobulins. Subsequent neuropsychological testing due to subjective cognitive complaints after immunotherapy revealed no objective cognitive deficits. Conclusions: We present the novel finding of an association between GAD65 autoantibodies in the serum and CSF with catatonia in a patient suffering from prediagnosed chronic schizophrenia. Due to the presence of CSF GAD65 antibodies and the catatonia factor in prediagnosed schizophrenia, we suspect that his catatonia has an autoimmune origin. Immunotherapy stabilized the catatonia that had initially responded to lorazepam treatment. Further research should be done to characterize patients' responses to immunotherapy and standard treatment in a large cohort of patients with GAD65 antibody-associated catatonia and schizophrenia.
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