The course of brain abnormalities in schizophrenia: can we slow the progression?

Journal of Psychopharmacology - Tập 26 Số 5_suppl - Trang 8-14 - 2012
N Van Haren1, Wiepke Cahn1, Hilleke E. Hulshoff Pol1, R.S. Kahn1
1Rudolf Magnus Institute of Neuroscience, Department of Psychiatry, University Medical Centre Utrecht, Utrecht, The Netherlands

Tóm tắt

There is convincing evidence that schizophrenia is characterized by progressive brain volume changes during the course of the illness. In a large longitudinal study it was shown that different age-related trajectories of brain tissue loss are present in patients compared with healthy subjects, suggesting that brain maturation that occurs in the third and fourth decade of life is abnormal in schizophrenia. Studies show that medication intake is an important confounding factor when interpreting brain volume (change) abnormalities. Atypical antipsychotics have been found to be related to smaller decreases in tissue loss. Moreover, independent of antipsychotic medication intake, the brain volume abnormalities appear associated to the outcome of the illness. Before being able to intervene with therapies and prevent the brain from shrinking, one has to understand the underlying mechanism of the progressive changes in the brains of schizophrenia patients.

Từ khóa


Tài liệu tham khảo

10.1016/j.schres.2003.12.002

10.1176/appi.ajp.160.8.1421

10.1001/archpsyc.65.11.1259

10.1192/bjp.bp.107.041467

10.1001/archpsyc.59.11.1002

10.1192/bjp.bp.105.015701

10.1016/S0140-6736(95)90441-7

10.1176/ajp.151.10.1430

10.1080/09540260701486647

10.1177/070674379704200105

10.1016/S0006-3223(97)00553-2

10.1038/sj.npp.1300603

10.1016/S0925-4927(98)00047-X

10.1016/j.pscychresns.2003.08.004

10.1038/sj.npp.1300710

10.1001/archpsyc.1991.01810350018003

10.1016/S0006-3223(99)00072-4

10.1001/archpsyc.64.7.772

10.1001/archpsyc.55.2.145

Haug JO, 1962, Acta Psychiatr Scand, 38, 1, 10.1111/j.1600-0447.1962.tb01780.x

10.1001/archpsyc.60.6.585

10.1093/schbul/sbm168

10.1176/appi.ajp.159.2.244

10.1016/j.neuroimage.2003.09.026

10.1001/archpsyc.58.12.1118

10.1176/appi.ajp.160.1.156

10.1001/archpsyc.60.8.766

10.1016/S0140-6736(94)90599-1

10.1038/sj.npp.1301233

10.1093/schbul/sbm158

10.1016/S0006-3223(01)01067-8

10.1001/archpsyc.62.4.361

10.1001/archpsyc.58.2.148

10.1093/schbul/14.4.515

10.1093/schbul/sbi034

10.1016/S0925-4927(01)00072-5

10.1001/archpsyc.55.3.215

10.1007/BF01837385

10.1016/S0893-133X(00)00172-X

10.1093/oxfordjournals.schbul.a006881

10.1016/S0006-3223(98)00281-9

10.1001/archpsyc.1995.03950220015005

10.1002/(SICI)1096-9861(19980316)392:3<402::AID-CNE9>3.0.CO;2-5

10.1016/S0920-9964(01)00163-3

10.1016/j.neubiorev.2010.01.016

10.1093/cercor/bhn152

10.1016/S0920-9964(03)00018-5

10.1016/j.biopsych.2007.01.004

10.1038/sj.npp.1301347

10.1192/bjp.166.6.750

10.1016/S0006-3223(98)00175-9

Westmoreland Corson PW, 1999, Am J Psychiatry, 156, 1200, 10.1176/ajp.156.8.1200

10.1093/schbul/sbm149

10.1016/S0920-9964(01)00175-X

10.1176/ajp.157.1.16