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Early trauma/dysmorphogenesis and adult neurodysfunction in schizophrenia

Ismail, Baher LU (2003)
Abstract
To measure the importance of early neurodevelopmental disturbance for schizophrenia, early trauma and dysmorphogenesis (i.e. obstetric complications (OCs), minor physical anomalies (MPAs), head circumference (HC) and dermatoglyphic characteristics) were studied in relationship to adult neurodysfunction (i.e. neurological abnormality (NA), neurocognitive dysfunction (NCGD), tardive dyskinesia (TD) and parkinsonism) in 60 schizophrenia patients, 21 of their non-ill siblings and 75 normal comparison subjects.



Patients showed reduced neonatal HC (nHC), increased rates of OCs, MPAs, NA and NCGD, and frequent signs of TD and parkinsonism. Siblings showed increased rates of MPAs, NA, and NCGD and frequent signs of TD,... (More)
To measure the importance of early neurodevelopmental disturbance for schizophrenia, early trauma and dysmorphogenesis (i.e. obstetric complications (OCs), minor physical anomalies (MPAs), head circumference (HC) and dermatoglyphic characteristics) were studied in relationship to adult neurodysfunction (i.e. neurological abnormality (NA), neurocognitive dysfunction (NCGD), tardive dyskinesia (TD) and parkinsonism) in 60 schizophrenia patients, 21 of their non-ill siblings and 75 normal comparison subjects.



Patients showed reduced neonatal HC (nHC), increased rates of OCs, MPAs, NA and NCGD, and frequent signs of TD and parkinsonism. Siblings showed increased rates of MPAs, NA, and NCGD and frequent signs of TD, implicating a general familial vulnerability for schizophrenia-related neurodysfunction. Patients differed from siblings by having reduced nHC and increased OCs, and higher rates of MPAs and adult neurodysfunction, signalling two different levels of early trauma/dysmorphogenesis and neurodysfunction: one characterising at-risk families in general, and another higher, disease-related level characterising the patient group. Early trauma/dysmorphogenesis was generally unrelated to adult neurodysfunction. HC in patients was reduced at birth but disproportionately large in males in adulthood. NA was related to level of global functioning in adulthood. Early trauma/dysmorphogenesis thus seems to initiate an early pathophysiological process, but additional factors influence adult neurodysfunction in schizophrenia. The findings in total would be consistent with a 'multi-hit' neurodevelopmental model of schizophrenia. The effective factors would vary from individual to individual and include both genetic and early/later environmental components. (Less)
Abstract (Swedish)
Popular Abstract in Swedish

Det finns alltmer bevis för att både genetiska och tidiga miljömässiga faktorer spelar en väsentlig roll i uppkomsten av schizofreni genom att påverka tidig neuroutveckling. För att kunna analysera betydelsen av tidig neuroutvecklingsavvikelse för uppkomst av schizofreni, har vi studerat tidiga traumata, dvs obstetriska komplikationer (OCs), samt dysmorfogenes, dvs lindriga medfödda missbildningar (MPAs), huvudomfång (HC) och finger/handflatsmönster (dermatoglyfiska egenskaper). Dessa har vidare satts i relation till "neurodysfunktion" i vuxen ålder, dvs neurologisk abnormitet (NA), neurokognitiv störning (NCGD), tardiv dyskinesi (TD) och parkinsonism. Studiepopulationen omfattar 60 patienter med... (More)
Popular Abstract in Swedish

Det finns alltmer bevis för att både genetiska och tidiga miljömässiga faktorer spelar en väsentlig roll i uppkomsten av schizofreni genom att påverka tidig neuroutveckling. För att kunna analysera betydelsen av tidig neuroutvecklingsavvikelse för uppkomst av schizofreni, har vi studerat tidiga traumata, dvs obstetriska komplikationer (OCs), samt dysmorfogenes, dvs lindriga medfödda missbildningar (MPAs), huvudomfång (HC) och finger/handflatsmönster (dermatoglyfiska egenskaper). Dessa har vidare satts i relation till "neurodysfunktion" i vuxen ålder, dvs neurologisk abnormitet (NA), neurokognitiv störning (NCGD), tardiv dyskinesi (TD) och parkinsonism. Studiepopulationen omfattar 60 patienter med schizofreni, 21 av deras mentalt friska syskon och 75 normala "kontroll" individer som saknar släktingar med psykos. Jämfört med kontrollgruppen, visade patienterna signifikant minskat HC vid födelsen, signifikant ökade OCs, MPAs, NA, och NCGD, samt frekventa tecken på TD och parkinsonism. Dessa fynd utgör starkt bevis för vikten av avvikande neuroutveckling för sjukdomen. Syskonen till patienter visade signifikant ökade MPAs, NA och NCGD, samt frekventa tecken på TD, vilket tyder på en generell familjär vulnerabilitet (sårbarhet) för neurodysfunktion som är kopplad till schizofreni. Patienterna skilde sig från sina syskon genom att ha signifikant minskat HC vid födelsen och ökat antal OCs i samband med födelsen och MPAs, samt en högre nivå av neurodysfunktion som vuxna. Detta talar för två olika nivåer av tidiga traumata/dysmorfogenes och neurodysfunktion: en nivå som gäller individerna i "risk familjer" i stort, och en annan, mer avvikande nivå som karakteriserar individer med sjukdomen. Tidiga traumata/dysmorfogenes var som regel inte relaterade till vuxen neurodysfunktion, på individnivå. Dessutom var patienternas HC minskat vid födelsen men oproportionellt stort (hos männen) i vuxen ålder. NA korrelerade till patientens globala funktionsnivå (psykiskt, socialt, yrkesmässigt) i vuxen ålder. Dessa fynd talar för att tidiga traumata/dysmorfogenes initierar en patofysiologisk process tidigt i livet vid schizofreni, men att det även finns andra faktorer som påverkar den specifika uttrycksformen av neurodysfunktionen i vuxen ålder. Resultaten i denna studie talar för en "multi-hit" neuroutvecklingsmodell vid schizofreni. På individnivå skulle olika genetiska förutsättningar såväl som miljömässiga faktorer kunna påverka denna utveckling. (Less)
Please use this url to cite or link to this publication:
author
supervisor
opponent
  • Prof. Murray, Robin, Institute of Psychiatry, London
organization
publishing date
type
Thesis
publication status
published
subject
keywords
Psychiatry, clinical psychology, klinisk psykologi, neurodevelopmental model, psychosomatics, Psykiatri, tardive dyskinesia, neurological abnormality, neurocognitive dysfunction, dermatoglyphics, head circumference, minor physical anomalies, Schizophrenia, obstetric complications, psykosomatik
pages
120 pages
publisher
Dept. of Psychiatric Epidemiology, Lund University Hospital USiL, S-221 85 Lund,
defense location
Segerfalkssalen, BMC, Lund
defense date
2003-12-01 09:15:00
ISBN
91-631-4318-6
language
English
LU publication?
yes
additional info
Article: B Ismail, E Cantor-Graae, TF McNeil. Neurological abnormalities in schizophrenic patients and their siblings. American Journal of Psychiatry 1998;155:84-89.BT Ismail, E Cantor-Graae, S Cardenal, TF McNeil. Neurological abnormalities in schizophrenia: clinical, etiological and demographic correlates. Schizophrenia Research 1998;30:229-238.B Ismail, E Cantor-Graae, TF McNeil. Minor physical anomalies in schizophrenic patients and their siblings. American Journal of Psychiatry 1998;155:1695-1702.B Ismail, E Cantor-Graae, TF McNeil. Minor physical anomalies in schizophrenia: cognitive, neurological and other clinical correlates. Journal of Psychiatric Research 2000;34:45-56.B Ismail, E Cantor-Graae, TF McNeil. Neurodevelopmental origins of tardivelike dyskinesia in schizophrenia patients and their siblings. Schizophrenia Bulletin 2001;27:629-642.E Cantor-Graae, B Ismail, TF McNeil. Are neurological abnormalities in schizophrenic patients and their siblings the result of perinatal trauma? Acta Psychiatrica Scandinavica 2000;101:142-147.E Cantor-Graae, B Ismail, TF McNeil. Neonatal head circumference and related indices of disturbed fetal development in schizophrenic patients. Schizophrenia Research 1998;32:191-199.
id
a86b4167-72a3-48da-91c5-f6e652c2e1f3 (old id 466367)
date added to LUP
2016-04-04 10:54:44
date last changed
2018-11-21 21:01:30
@phdthesis{a86b4167-72a3-48da-91c5-f6e652c2e1f3,
  abstract     = {{To measure the importance of early neurodevelopmental disturbance for schizophrenia, early trauma and dysmorphogenesis (i.e. obstetric complications (OCs), minor physical anomalies (MPAs), head circumference (HC) and dermatoglyphic characteristics) were studied in relationship to adult neurodysfunction (i.e. neurological abnormality (NA), neurocognitive dysfunction (NCGD), tardive dyskinesia (TD) and parkinsonism) in 60 schizophrenia patients, 21 of their non-ill siblings and 75 normal comparison subjects.<br/><br>
<br/><br>
Patients showed reduced neonatal HC (nHC), increased rates of OCs, MPAs, NA and NCGD, and frequent signs of TD and parkinsonism. Siblings showed increased rates of MPAs, NA, and NCGD and frequent signs of TD, implicating a general familial vulnerability for schizophrenia-related neurodysfunction. Patients differed from siblings by having reduced nHC and increased OCs, and higher rates of MPAs and adult neurodysfunction, signalling two different levels of early trauma/dysmorphogenesis and neurodysfunction: one characterising at-risk families in general, and another higher, disease-related level characterising the patient group. Early trauma/dysmorphogenesis was generally unrelated to adult neurodysfunction. HC in patients was reduced at birth but disproportionately large in males in adulthood. NA was related to level of global functioning in adulthood. Early trauma/dysmorphogenesis thus seems to initiate an early pathophysiological process, but additional factors influence adult neurodysfunction in schizophrenia. The findings in total would be consistent with a 'multi-hit' neurodevelopmental model of schizophrenia. The effective factors would vary from individual to individual and include both genetic and early/later environmental components.}},
  author       = {{Ismail, Baher}},
  isbn         = {{91-631-4318-6}},
  keywords     = {{Psychiatry; clinical psychology; klinisk psykologi; neurodevelopmental model; psychosomatics; Psykiatri; tardive dyskinesia; neurological abnormality; neurocognitive dysfunction; dermatoglyphics; head circumference; minor physical anomalies; Schizophrenia; obstetric complications; psykosomatik}},
  language     = {{eng}},
  publisher    = {{Dept. of Psychiatric Epidemiology, Lund University Hospital USiL, S-221 85 Lund,}},
  school       = {{Lund University}},
  title        = {{Early trauma/dysmorphogenesis and adult neurodysfunction in schizophrenia}},
  year         = {{2003}},
}