Hypofrontality With Positive Anti-NMDA Receptor Antibodies

Maung, Hane Htut; Dell'Erba, Gaetano

doi:10.1176/appi.neuropsych.11070164

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…Still, parts of some studies do not show any abnormalities, e.g., [56]. Some patients suffering from the initial phase of NMDAR autoimmune encephalitis with NR1 antibodies may exhibit schizophrenia-like psychotic behavior [60,61] or symptoms of hypofrontality [62], however, the vast majority of recent studies do not confirm the presence of IgG-NR1 antibodies in schizophrenia [63,64].…”

Section: Glutamatergic Signaling and Cognitive Deficits In Schizopmentioning

confidence: 99%

NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality

Krzystanek¹,

Pałasz²

2019

IJMS

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Schizophrenia is a chronic mental disease, affecting around 1% of the general population. Schizophrenia is characterized by productive, negative, affective, and disorganization symptoms, and cognitive deficits. Cognitive deficits prevail in most of the schizophrenia patients and are one of the most disabling symptoms. They usually occur before the acute episode of the disease and tend to become chronic with no satisfactory treatment from antipsychotic drugs. Because of their early manifestation in patients’ lives, cognitive deficits are suggested to be the primary symptom of schizophrenia. The pathogenesis of cognitive deficits in schizophrenia is not fully understood. They are linked with hypofrontality, which is a decrease in blood flow and glucose metabolism in the prefrontal lobe of schizophrenia-suffering patients. Hypofrontality is linked with disturbances of the corticolimbothalamic circuit, important for cognition and memory in humans. The circuit consists of a group of neuroanatomic structures and hypothetically any disturbance in them may result in cognitive deficits. We present a translational preclinical model of understanding how antipsychotic medication may decrease the N-methyl-D-aspartic acid (NMDA) receptors’ activity and produce dysfunctions in the corticolimbothalamic circuit and hypofrontality. From several pharmacological experiments on rats, including mainly our own recent findings, we collected data that suggest that antipsychotic medication may maintain and escalate hypofrontality in schizophrenia, decreasing NMDA receptor activity in the corticolimbothalamic circuit in the human brain. We discuss our findings within the literature of the subject.

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Section: Glutamatergic Signaling and Cognitive Deficits In Schizopmentioning

confidence: 99%

NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality

Krzystanek¹,

Pałasz²

2019

IJMS

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Simple Schizophrenia

et al. 2019

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Clustering of symptoms to characterize simple schizophrenia is still debated, and support is needed for the characterization of simple schizophrenia as a syndrome. We conducted a systematic review to identify all cases of simple schizophrenia published until December 2017. We identified 42 cases of simple schizophrenia, 57% of which met all three diagnostic criteria (ICD-10, DSM-4 research criteria, and Black and Boffeli's criteria for simple schizophrenia). The mean age at first contact with clinical services was 30.1 (SD = 11.6) years, with a mean delay of 7.4 (SD = 6.8) years from symptom onset to first presentation. An insidious onset and negative symptoms were characteristic features in all cases. Social withdrawal, alogia, blunted affect, lack of initiative/interest, and functional impairment were found in more than 85% of cases. Our findings contribute to greater awareness and understanding of simple schizophrenia, and have the potential to reawaken interest in this clinically distinct subgroup.

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Hypofrontality With Positive Anti-NMDA Receptor Antibodies

Cited by 2 publications

References 5 publications

NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality

NMDA Receptor Model of Antipsychotic Drug-Induced Hypofrontality

Simple Schizophrenia

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