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Mental Health and Neurobehavioral Function in Young Adult Offspring of Women with a History of Psychosis and Control Offspring

Schubert, Erland LU (2004)
Abstract
Schizophrenia is now generally considered to be a brain disease resulting from disturbed neurodevelopment, mediated by genetic and/or adverse events in utero and/or in early childhood. This process manifests itself in schizophrenia in young adulthood, when the brain completes its maturation. The background and development of affective psychosis have been less extensively investigated. Our aim was to study mental health and neurobehavioral characteristics in 75 young adult offspring of mothers with a history of psychosis (38 offspring with heightened risk for schizophrenia, and 37 with heightened risk for affective psychosis), and 91 normal-risk offspring of mothers with no history of psychosis. In a 93%-effective (total n=166) follow-up of... (More)
Schizophrenia is now generally considered to be a brain disease resulting from disturbed neurodevelopment, mediated by genetic and/or adverse events in utero and/or in early childhood. This process manifests itself in schizophrenia in young adulthood, when the brain completes its maturation. The background and development of affective psychosis have been less extensively investigated. Our aim was to study mental health and neurobehavioral characteristics in 75 young adult offspring of mothers with a history of psychosis (38 offspring with heightened risk for schizophrenia, and 37 with heightened risk for affective psychosis), and 91 normal-risk offspring of mothers with no history of psychosis. In a 93%-effective (total n=166) follow-up of this longitudinally studied sample, mental disturbance, neurological abnormality and neuropsychological performance were blindly investigated at mean 22.4 yr of age. The subjects were previously assessed with a standard test of vision at 4 yr of age, and neurological examinations were blindly performed in infancy and at 6 yr of age. · Offspring at high-risk for schizophrenia showed more (a) mental disturbance (DSM-III-R Axis I and Axis II disorders, poor global functioning, high Symptom Check List-90 (SCL-90) scores and a history of mental health care and psychopharmacological medication), (b) diverse neurological abnormalities, and (c) neuropsychological impairments (on verbal memory, selective attention and grammatical reasoning tests). A neurobehaviorally deviant subgroup was identified only among this offspring group. · Offspring at high-risk for affective psychosis showed high SCL-90 scores, and more frequent poor functioning and receipt of mental health care, with an increase only in Axis I depressive disorders. No increase of neurological abnormality or neuropsychological impairments was found for this group. · Neurological abnormalities at 22 yr were associated with (a) neurological abnormalities at 6 yr of age, but not in infancy, and with (b) multiple adult neuropsychological functions in offspring at high-risk for schizophrenia and in normal-risk offspring, but not among offspring at high-risk for affective psychosis. · Offspring mental disturbance and neurobehavioral characteristics were generally similar when defining offspring risk by maternal “core” psychosis cases vs. additional maternal “psychosis spectrum” cases. · Offspring neurobehavioral deficits were related to offspring schizophrenia-spectrum disorder in a different manner from that for offspring affective disorders. · Visual dysfunction at 4 yr of age predicted offspring schizophrenia-spectrum disorders but no other psychiatric disorders in adulthood. Visual dysfunction at 4 yr of age was significantly related to neurological abnormality at 6 yr of age, suggesting a neurodevelopmental basis for schizophrenia-spectrum disorders. · The findings in total show a different pattern of mental disturbance and neurobehavioral characteristics in offspring with genetic high-risk for schizophrenia, in comparison with offspring at high-risk for affective psychosis and offspring at normal-risk. This suggests that schizophrenia may be part of a probably genetically mediated neurobehavioral syndrome and a consequence of disturbed neurodevelopment that belongs to a different neurobiological spectrum from that for affective disorders. Nevertheless, neurobehavioral deviations in general are not pathognomonic for schizophrenia-spectrum disorders or other psychiatric disturbance. (Less)
Abstract (Swedish)
Popular Abstract in Swedish

Schizofreni anses idag av många forskare som en neuroutvecklingssjukdom, orsakad av genetiska och/eller skadliga händelser under fostertiden, kring förlossningen och i tidig barndom som leder till en avvikande neurologisk utveckling. Denna process manifesterar sig i schizofreni senare i vuxen ålder när hjärnan genomgår sin slutliga mognad. Bakgrunden och utvecklingsförloppet för affektiv psykos är mindre utforskade. Vår målsättning var att studera mental hälsa och olika tecken på neurodysfunktion hos 75 barn till mödrar med anamnes för psykossjukdom (38 barn till mödrar med schizofreni-spektrum psykos, 37 barn till mödrar med affektiv-spektrum psykos), samt 91 barn till mödrar utan psykossjukdom.... (More)
Popular Abstract in Swedish

Schizofreni anses idag av många forskare som en neuroutvecklingssjukdom, orsakad av genetiska och/eller skadliga händelser under fostertiden, kring förlossningen och i tidig barndom som leder till en avvikande neurologisk utveckling. Denna process manifesterar sig i schizofreni senare i vuxen ålder när hjärnan genomgår sin slutliga mognad. Bakgrunden och utvecklingsförloppet för affektiv psykos är mindre utforskade. Vår målsättning var att studera mental hälsa och olika tecken på neurodysfunktion hos 75 barn till mödrar med anamnes för psykossjukdom (38 barn till mödrar med schizofreni-spektrum psykos, 37 barn till mödrar med affektiv-spektrum psykos), samt 91 barn till mödrar utan psykossjukdom. 93% (166) av dessa prospektivt studerade barn följdes nyligen upp vid 22 års ålder och ”blint” studerades med avseende på mental hälsa, neurologisk abnormitet och neuropsykologisk funktion. Barnen hade tidigare undersökts med syn test vid 4 års ålder och neurologisk undersökning i nyföddhetsperioden och vid 6 års ålder. · Barn med ökad risk för schizofreni hade ökad förekomst av (a) mentala störningar (DSM-III-R Axel I och Axel II störningar, lägre global funktionsnivå, mer lindriga psykiska symptom och ökad förekomst av professionell psykisk hjälp och psykofarmaka), (b) neurologisk abnormitet, samt (c) neuropsykologiska störningar (i verbalt minne, selektiv uppmärksamhet och exekutiv funktion). En subgrupp med ökad neurodysfunktion kunde identifieras endast bland dessa barn. · Barn med ökad risk för affektiv psykos hade ökad förekomst av Axel I psykiatrisk diagnos, särskilt depression (men inte Axel II personlighetsstörning), mer lindriga psykiska symptom, lägre global funktionsnivå och ökad förekomst av professionell psykisk hjälp. Ingen ökad förekomst av neurologisk abnormitet eller neuropsykologiska störningar fanns i denna grupp. · Neurologisk abnormitet i vuxen ålder var korrelerad till (a) neurologisk abnormitet vid 6 års ålder, men inte i nyföddhetsperioden och till (b) ett flertal neuropsykologiska funktioner bland barn med ökad risk för schizofreni och barn med normal risk, men inte bland barn med risk för affektiv psykos. · Att definiera barnens risk genom att utvidga maternell psykos till att inkludera ”spektrum psykos” (jämfört med ”kärnpsykosgrupperna”) medförde samma resultat avseende barnens mentala störning och tecken på neurodysfunktion. · Barnens neurodysfunktion var relaterat till schizofrent-spektrum störningar på ett annat sätt än till affektiva störningar hos barnen. · Visuell dysfunktion vid 4 års ålder predicerade schizofrent-spektrum störningar i vuxen ålder, men inte någon annan psykiatrisk diagnos. Vidare var visuell dysfunktion vid 4 års ålder signifikant relaterad till neurologisk abnormitet i 6 års åldern, talande för en neuroutvecklingsgrund för schizofrent-spektrum störningar. · Sammantaget visar fynden ett annat mönster av mentala störningar och neurodysfunktion bland barn med genetiskt ökad risk för schizofreni jämfört med barn med ökad risk för affektiv psykos och barn med normal risk. Detta tyder på att schizofreni möjligen är en del av ett sannolikt genetiskt medierat neurodysfunktionellt syndrom och en konsekvens av en störd neurologisk utveckling som tillhör ett annat neurobiologiskt spektrum i jämförelse med affektiv sjukdom. Neurodysfunktion är dock inte i allmänhet patognomont för schizofrent-spektrum störningar eller andra psykiatriska störningar. (Less)
Please use this url to cite or link to this publication:
author
supervisor
opponent
  • Professor Murray, Robin, Institute of Psychiatry, London
organization
publishing date
type
Thesis
publication status
published
subject
keywords
Psychiatry, klinisk psykologi, Psykiatri, psykosomatik, clinical psychology, visual dysfunction, neuropsychological function, neurological abnormality, neurodevelopment, mental disturbance, high-risk, genetic, schizophrenia, affective psychosis, psychosomatics
pages
160 pages
publisher
Erland Schubert, Dept. of Psychiatric Epidemiology, Barngatan 2, Universitetssjukhuset i Lund USiL, S-221 85 Lund, Sweden,
defense location
Segerfalkssalen, BMC, Lund
defense date
2004-11-12 13:00:00
ISBN
91-631-4319-4
language
English
LU publication?
yes
additional info
Article: Schubert EW & McNeil TF.Prospective study of adult mental disturbance in offspring of women with psychosis.Archives of General Psychiatry 2003;60:473-480. Article: Schubert EW & McNeil TF.Prospective study of neurological abnormalities in offspring of women with psychosis: birth to adulthood.American Journal of Psychiatry 2004;161:1030-1037. Article: Schubert EW & McNeil TF.Neuropsychological impairment and its neurological correlates in adult offspring with heightened risk for schizophrenia and affective psychosis.American Journal of Psychiatry, accepted for publication. Article: Schubert EW & McNeil TF.The association between schizophrenia-spectrum vs. affective disorder and neurobehavioral deficits in adult offspring with heightened risk for psychosis.Submitted for publication 2004. Article: Schubert EW, Henriksson KM, McNeil TF.A prospective study of visual dysfunction in early childhood and schizophrenia-spectrum disorders in adulthood.Submitted for publication 2004.
id
1989b66d-a05d-46db-959f-b674c11c0329 (old id 467439)
date added to LUP
2016-04-04 12:17:41
date last changed
2018-11-21 21:10:08
@phdthesis{1989b66d-a05d-46db-959f-b674c11c0329,
  abstract     = {{Schizophrenia is now generally considered to be a brain disease resulting from disturbed neurodevelopment, mediated by genetic and/or adverse events in utero and/or in early childhood. This process manifests itself in schizophrenia in young adulthood, when the brain completes its maturation. The background and development of affective psychosis have been less extensively investigated. Our aim was to study mental health and neurobehavioral characteristics in 75 young adult offspring of mothers with a history of psychosis (38 offspring with heightened risk for schizophrenia, and 37 with heightened risk for affective psychosis), and 91 normal-risk offspring of mothers with no history of psychosis. In a 93%-effective (total n=166) follow-up of this longitudinally studied sample, mental disturbance, neurological abnormality and neuropsychological performance were blindly investigated at mean 22.4 yr of age. The subjects were previously assessed with a standard test of vision at 4 yr of age, and neurological examinations were blindly performed in infancy and at 6 yr of age. · Offspring at high-risk for schizophrenia showed more (a) mental disturbance (DSM-III-R Axis I and Axis II disorders, poor global functioning, high Symptom Check List-90 (SCL-90) scores and a history of mental health care and psychopharmacological medication), (b) diverse neurological abnormalities, and (c) neuropsychological impairments (on verbal memory, selective attention and grammatical reasoning tests). A neurobehaviorally deviant subgroup was identified only among this offspring group. · Offspring at high-risk for affective psychosis showed high SCL-90 scores, and more frequent poor functioning and receipt of mental health care, with an increase only in Axis I depressive disorders. No increase of neurological abnormality or neuropsychological impairments was found for this group. · Neurological abnormalities at 22 yr were associated with (a) neurological abnormalities at 6 yr of age, but not in infancy, and with (b) multiple adult neuropsychological functions in offspring at high-risk for schizophrenia and in normal-risk offspring, but not among offspring at high-risk for affective psychosis. · Offspring mental disturbance and neurobehavioral characteristics were generally similar when defining offspring risk by maternal “core” psychosis cases vs. additional maternal “psychosis spectrum” cases. · Offspring neurobehavioral deficits were related to offspring schizophrenia-spectrum disorder in a different manner from that for offspring affective disorders. · Visual dysfunction at 4 yr of age predicted offspring schizophrenia-spectrum disorders but no other psychiatric disorders in adulthood. Visual dysfunction at 4 yr of age was significantly related to neurological abnormality at 6 yr of age, suggesting a neurodevelopmental basis for schizophrenia-spectrum disorders. · The findings in total show a different pattern of mental disturbance and neurobehavioral characteristics in offspring with genetic high-risk for schizophrenia, in comparison with offspring at high-risk for affective psychosis and offspring at normal-risk. This suggests that schizophrenia may be part of a probably genetically mediated neurobehavioral syndrome and a consequence of disturbed neurodevelopment that belongs to a different neurobiological spectrum from that for affective disorders. Nevertheless, neurobehavioral deviations in general are not pathognomonic for schizophrenia-spectrum disorders or other psychiatric disturbance.}},
  author       = {{Schubert, Erland}},
  isbn         = {{91-631-4319-4}},
  keywords     = {{Psychiatry; klinisk psykologi; Psykiatri; psykosomatik; clinical psychology; visual dysfunction; neuropsychological function; neurological abnormality; neurodevelopment; mental disturbance; high-risk; genetic; schizophrenia; affective psychosis; psychosomatics}},
  language     = {{eng}},
  publisher    = {{Erland Schubert, Dept. of Psychiatric Epidemiology, Barngatan 2, Universitetssjukhuset i Lund USiL, S-221 85 Lund, Sweden,}},
  school       = {{Lund University}},
  title        = {{Mental Health and Neurobehavioral Function in Young Adult Offspring of Women with a History of Psychosis and Control Offspring}},
  year         = {{2004}},
}