Td. Cannon, ABNORMALITIES OF BRAIN STRUCTURE AND FUNCTION IN SCHIZOPHRENIA - IMPLICATIONS FOR ETIOLOGY AND PATHOPHYSIOLOGY, Annals of medicine, 28(6), 1996, pp. 533-539
In vivo imaging and post-mortem neuropathology studies have detected a
variety of abnormalities in brain function and structure in patients
with schizophrenia. Current models of the neural mechanisms involved f
ocus primarily on frontal and medial temporal lobe structures and thei
r interconnections, because deficits in these systems are relatively p
rominent against a background of generalized cerebral dysfunction, and
because individuals with acquired lesions in these areas show many of
the symptoms characteristic of schizophrenia. Family and twin studies
have demonstrated similar abnormalities in some of the unaffected bio
logical relatives of schizophrenics, indicating that some of these neu
ropathological changes are mediated in part by genetic predisposition
to the disorder, Further, obstetric complications are associated with
an increased risk for phenotypic schizophrenia and with greater severi
ty of its neuropathological features in individuals at elevated geneti
c risk. These latter findings, combined with evidence of heterotopic d
isplacement of neurones in temporolimbic and frontal regions and evide
nce that cognitive dysfunction during childhood precedes schizophrenia
, imply that at least some of these brain abnormalities are neurodevel
opmental in origin, The view emerging from this work is that schizophr
enia is a brain disease the neuropathological features of which result
at least in part from the unique and interacting influences of geneti
c factors and adverse obstetric events in utero.