Origine et renouveau du concept de démence dans la schizophrénie

An increasing amount of current literature on schizophrenia is devoted to the role dementia may play in its course. This renewed interest had the way paved by the very history of the dementia concept. Before Kraepelin coined the term of "dementia praecox" as the hallmark of a common terminal state for hebephrenia, catatonia and paranoid psychosis, dementia acquired, as soon as the end of the 18th-century its cognitive meaning. In France, Pinel yet spoke of an "abolition of thinking", but in the same time considered dementia as one of the four forms of mental alienation, alongside with mania, melancolia and idiotism. During the 19-th century dementia was defined as an acquired deficit of intelligence supported by a brain disease, but which could be due to a mental illness. Owing to progress in neuropathology, several diseases such as Alzheimer or Pick illnesses were identified as causes of dementia, so that the concept was annexed by neurologists and received less interest from psychiatrists, during the last century. That seemed to change, twenty years ago, when clinical discussions emerged around the issues raised by depressive (pseudo) dementia. In psychiatry, the broader conceptualization of schizophrenia introduced by Bleuler in 1911 has not been widely adopted, many authors having been continuing sharing the Kraepelinian view that, at least one form of the disease, was a chronic progressive illness leading to severe impairments in cognitive and social functioning. Historical variations in diagnostic criteria used for schizophrenia had an impact on the way psychiatrists assessed outcome of the disease, leading some of them to consider schizophrenia as a nosological category without natural boundaries and propose to abandon the concept. However the use of narrow criteria is currently prevailing. Advances in neurocognitive testing and changes in theoretical models allowed, at the end of the last century, to document that schizophrenia was characterized by a broadly based cognitive impairment. Deficits were found in various domains: global and selective verbal memory, non-verbal memory, bilateral and unilateral motor performance, visual and auditory attention, general intelligence, spatial ability, executive function, language and interhemispheric tactile-transfer test performance. The hypothesis according to which the vast majority of these cognitive deficits had a neurodevelopmental origin was recently challenged by findings from longitudinal neurocognitive and neuroimaging studies. Some studies, for example, show that if first episode patients have smaller left hippocampal volumes as compared with controls, there is also an association of smaller right hippocampal volumes with increased illness duration in chronic schizophrenia. Others have shown that neuropsychological evaluations before treatment permitted differentiation of primary deficits from changes secondary to medication or chronicity. Clinicians reported that in some cases of chronic schizophrenic patients, dementia could be a complication of the disease, sharing common neuropsychological features with frontotemporal dementia. The effect of age was discussed too, as seeming to play sometimes a part. Even if the cause of the degenerative process that appears to occur in the brains of some schizophrenic patients remains largely unknown, advances in neuropathological models of degeneration in the brain as well as in mechanisms and factors underlying its process, gave rise to hypotheses liable to explain how degenerative dementia could occur in schizophrenia. Excess products of membrane degeneration which was evidenced by magnetic resonance spectroscopy suggests increased apoptosis in some schizophrenic patients. Deficits in neurotrophic factors, free radical oxidation, excess glutamate activity have been implicated as well as abnormalities in dopamine and cortisol metabolism. Growing evidence that some newer antipsychotics seem capable to interfere with these processes, slowing down their progression and even stopping it, has contributed to the renewal of the concept, opening new avenues to preventive strategies in the treatment of schizophrenia.