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catatonia/inflamación
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Micro(glial)-managing executive function: white matter inflammation drives catatonia.
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White matter abnormalities are prevalent in neuropsychiatric disorders such as schizophrenia, but it is unclear whether these abnormalities represent a cause or consequence of these disorders. Reduced levels of the myelin protein 2'-3'-cyclic nucleotide 3'-phosphodiesterase (CNP) are associated with
Contemporary encephalitis lethargica presenting with agitated catatonia, stereotypy, and dystonia-parkinsonism.
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Encephalitis lethargica (EL) syndrome was classically described by Von Economo and has somnolent-ophthalmoplegic, hyperkinetic, and amyostatic-akinetic forms. We describe 2 recent cases of EL characterized by an acute encephalitis with mixed movement disorders (dystonia-Parkinsonism plus stereotypy)
Catatonia and the immune system: a review.
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Catatonia is a psychomotor disorder featuring stupor, posturing, and echophenomena. This Series paper examines the evidence for immune dysregulation in catatonia. Activation of the innate immune system is associated with mutism, withdrawal, and psychomotor retardation, which constitute the
A myelin gene causative of a catatonia-depression syndrome upon aging.
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Severe mental illnesses have been linked to white matter abnormalities, documented by postmortem studies. However, cause and effect have remained difficult to distinguish. CNP (2',3'-cyclic nucleotide 3'-phosphodiesterase) is among the oligodendrocyte/myelin-associated genes most robustly reduced on
Genetically induced brain inflammation by Cnp deletion transiently benefits from microglia depletion.
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Reduced expression of 2'-3'-cyclic nucleotide 3'-phosphodiesterase (Cnp) in humans and mice causes white matter inflammation and catatonic signs. These consequences are experimentally alleviated by microglia ablation via colony-stimulating factor 1 receptor (CSF1R) inhibition using
[The neuroleptic malignant syndrome].
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METHODS
A 22-year-old oligophrenic patient had on several occasions over several months been given various neuroleptics (haloperidol, benperidol, levomepromazine) for exacerbations of paranoid schizophrenia. For a few days before hospitalization he had become quiet and withdrawn, but on the day of
[Malignant neuroleptic syndrome and polyserositis associated to clozapine use: report of one case].
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Malignant neuroleptic syndrome is a complication of antipsychotic medication use. Clozapine use is also associated with polyserositis and eosinophilia. We report a 17 years old female treated with clozapine, valproic acid, lithium carbonate and lorazepam that consulted in the emergency room for
Anti-N-Methyl-D-Aspartate-Receptor Encephalitis: A 10-Year Follow-Up
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Background: Anti-N-methyl-D-aspartate-receptor (NMDA-R) encephalitis is an autoimmune disease of the brain first described in 2007. The aim of this paper is to present a 10-year follow-up case history.
Case presentation: The
Licofelone attenuates MPTP-induced neuronal toxicity: behavioral, biochemical and cellular evidence.
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Neuroinflammation and oxidative stress play critical role in the pathophysiology of neurodegenerative diseases including Parkinson's disease (PD). Recent reports indicate the beneficial effect of anti-inflammatory drugs in attenuating the progression of PD. Therefore, the present study is aimed to
Novel Antineuronal Autoantibodies With Somatodendritic Staining Pattern in a Patient With Autoimmune Psychosis
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Background: Autoimmune encephalitis, such as anti-NMDA-receptor encephalitis, typically presenting with subacute onset of neuropsychiatric symptoms, can be detected by antineuronal autoantibodies or inflammatory changes in the
[Features of the immune profile of schizophrenic patients with catatonic syndrome]
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Objective: An analysis of inflammatory and autoimmune markers in schizophrenic patients with- and without catatonic symptoms in comparison to healthy controls.
Material and methods:
Pharmacological Treatment of Chemotherapy-Induced Neuropathic Pain: PPARγ Agonists as a Promising Tool.
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Chemotherapy-induced neuropathic pain (CINP) is one of the most severe side effects of anticancer agents, such as platinum- and taxanes-derived drugs (oxaliplatin, cisplatin, carboplatin and paclitaxel). CINP may even be a factor of interruption of treatment and consequently increasing the risk of
Higher Serum C-Reactive Protein Levels in Catatonic Patients: A Comparison to Non-catatonic Patients and Healthy Controls.
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Catatonia is a psychomotor syndrome defined by a constellation of predominantly motor symptoms. The aim of the present study was to determine whether recently admitted psychiatric patients with catatonia exhibited higher serum C-reactive protein (hs-CRP) levels compared to non-catatonic psychiatric
Autoantibody-associated movement disorders.
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Autoantibodies to the extracellular domain of neuronal proteins cause different neurological conditions with movement disorders as a prominent feature. We reviewed the literature of autoantibody-mediated and autoantibody-associated diseases focusing on anti-N-methyl-D-aspartate receptor (NMDAR)
Microglia ablation alleviates myelin-associated catatonic signs in mice.
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The underlying cellular mechanisms of catatonia, an executive "psychomotor" syndrome that is observed across neuropsychiatric diseases, have remained obscure. In humans and mice, reduced expression of the structural myelin protein CNP is associated with catatonic signs in an age-dependent manner,
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