Brain Imaging and Function — The Balance of the Century

Abstract

Although schizophrenia (as dementia praecox) was separated from the broad mass of psychotic illness more than 100 years ago (Kraepelin 1896) imaging studies of the disorder did not begin for another three decades. The idea that schizophrenia was associated with structural brain changes had, however, been put forward earlier. In 1891 Sir Thomas Clouston wrote of central nervous system abnormalities as a feature of the disorder that he called adolescent insanity and later considered as included in Kraepelin’s concept of dementia praecox. In 1907, Kraepelin wrote (with reference to dementia praecox/schizophrenia) ‘the fact is decisive that the morbid anatomy has disclosed not simple inadequacy of the nervous system but destructive morbid processes as the background of the clinical picture.’ He quoted the work of Alzheimer and Nissl, writing ‘Alzheimer has described deep-spreading changes in the cortical cells, especially in the deep layers: the nuclei are very much swollen, the nuclear membrane greatly wrinkled, the body of the cell considerably shrunk with a tendency to degeneration. Nissl invariably saw widespread cellular disease.’ Many early investigators of the underlying cause of schizophrenia concentrated upon neuropathology, and indeed the notion that the neuropathological changes were determined by maldevelopment of the brain was widespread (Mackenzie 1912; Turner 1912; Rosanoff 1914; Southard 1915).