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No neurochemical evidence of neuronal injury or glial activation in children with Pediatric Acute-onset Neuropsychiatric Syndrome: An explorative pilot study.

Johnson, Mats, 1956 (author)
Gothenburg University,Göteborgs universitet,Gillbergcentrum,Gillberg Neuropsychiatry Centre
Fernell, Elisabeth, 1948 (author)
Gothenburg University,Göteborgs universitet,Gillbergcentrum,Gillberg Neuropsychiatry Centre
Gillberg, Christopher, 1950 (author)
Gothenburg University,Göteborgs universitet,Gillbergcentrum,Gillberg Neuropsychiatry Centre
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Fasth, Anders, 1945 (author)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper, Avdelningen för pediatrik,Institute of Clinical Sciences, Department of Pediatrics
Dinkler, Lisa (author)
Gothenburg University,Göteborgs universitet,Gillbergcentrum,Gillberg Neuropsychiatry Centre
Blennow, Kaj, 1958 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Zetterberg, Henrik, 1973 (author)
Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
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 (creator_code:org_t)
2021-04-16
2021
English.
In: The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry. - : Informa UK Limited. - 1814-1412. ; 22:10, s. 800-804
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Summary Objective: Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) is characterized by an acute onset of obsessive compulsive disorder, combined with at least two other neuropsychiatric symptoms with acute onset. Diagnostic criteria also require that no specific medical etiology is identified. Although there are no verified etiological biomarkers, PANS is assumed to be a neuroinflammatory disorder with a possible autoimmune etiology. Neurochemical markers such as neurofilament light (NfL, a neuronal injury marker) and glial fibrillary acidic protein (GFAP, an astrocytic activation marker) have not been published for this patient group. Method: Blood samples from 17 children meeting diagnostic criteria for PANS, after assessment at a child neuropsychiatry clinic were analysed for serum concentrations of NfL and GFAP. Ten age-matched children without any neurological or psychiatric disorder served as a comparison group. Results: No difference was found in mean NfL and mean GFAP serum concentrations between children with PANS and controls. Conclusion: Neuronal injury and astrocyte activation do not seem to be a major event in PANS. The study group was small, and even if findings may be reassuring for parents and patients, they should be interpreted with caution and verified in larger cohort and possibly with other markers in both serum and CSF.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Pediatrik (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Pediatrics (hsv//eng)

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