| Literature DB >> 31649298 |
Cecilie Koldbæk Lemvigh1,2, Jens Richardt Møllegaard Jepsen3,4, Birgitte Fagerlund3,5, Anne Katrine Pagsberg4,6, Birte Yding Glenthøj3,6, Jacob Rydkjær3,4, Bob Oranje3,7.
Abstract
Numerous studies have demonstrated impaired sensory gating in schizophrenia and this impairment has been proposed as a candidate biomarker for the disorder. The typical age of onset for schizophrenia is early adulthood, however a sizable group of patients present with psychotic symptoms before the age of 18, commonly referred to as early-onset psychosis (EOP). How an earlier onset influences sensory gating is currently unknown. Impaired sensory gating may not be specific to psychosis, but rather a shared disturbance of neurodevelopmental disorders, such as attention deficit/hyperactivity disorder (ADHD). Therefore, the current study investigated P50 suppression in young adolescents (12-17 years old) with either EOP (N = 55) or ADHD (N = 28) and age and gender matched healthy controls (HC) (N = 71). In addition to P50 suppression, N100 and P200 suppression data were also analyzed. No significant group differences in either raw mean P50 amplitude or mean P50 gating ratios were observed between EOP, ADHD, and HC. Additionally, we observed no P50 suppression deficit in those EOP patients diagnosed with schizophrenia (N = 39). Similarly, we observed no differences in N100 or P200 between the three groups. Healthy levels of P50 suppression were found in both patient groups. The results are in line with some previous studies showing healthy levels of P50 suppression in the early phases of schizophrenia. Our findings do not support P50 sensory gating as a valid biomarker for EOP or ADHD.Entities:
Mesh:
Year: 2019 PMID: 31649298 PMCID: PMC7021818 DOI: 10.1038/s41386-019-0555-9
Source DB: PubMed Journal: Neuropsychopharmacology ISSN: 0893-133X Impact factor: 7.853