The biology of schizophrenia

Conclusions

Genes may be relevant not only to predisposition but also to the type of schizophrenic illness which occur, and determine whether symptoms of the type I or type II syndromes or a combination of the two are the major manifestations. Both syndromes, howerver, might be caused by a single agent, e.g.a. virus. Thus, amongst the population of patients at risk there is a group who experience a primary neurochemical disturbance (e.g. of dopaminergic transmission). This becomes manifest in positive symptoms (delusions, hallucinations and thought disorder) and might result from an affinity of the virus for a particular neurochemical structure (e.g. the D₂ dopamine receptor or a molecule concerned in its regulation). Within this population however, is a sub-group that is predisposed to a more malignant and widespread disease. In these patients the virus gains further footholds in the nervous system, with the consequence that the disease acquires the characteristics of a chronic encephalitis. It is in these cases that there is evidence of structural change (although the site of the presumed cell loss has yet to be determined) and when present this change is associated with intellectual impairment and negative symptoms (the type II syndrome).

Thus the disturbance underlying the type I syndrome is a neurochemical one which accounts for the reversibility of some schizophrenic symptoms and illnesses, and their response to neuroleptic drugs. It is compatible with Bleuler's view of schizophrenia as a functional psychosis which can be clearly distinguished from dementia. The change underlying the type II syndrome is progressive and irreversible and accounts for poor long-term outcome. To this form of illness Kraepelin's term dementia praecox can be applied with the term dementia retaining its contemporary connotation of organic psychosis.