PubMed · 7829045
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K W Hammond, M Snowden, T Adkins, J J O'Brien. 1994. Computerized TD reminders.. https://doi.org/10.1176/ps.45.10.1043
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The great diversity of schizophrenic symptoms rules out one simple etiological explanation. However,impairment of information processing, including disruption of sensorimotor gating, is a consistent finding in schizophrenic patients. Dysfunction in sensorimotor gating is believed to be the result of different developmentally or environmentally caused disturbances involving the neural trajectories involved in information processing. Psychopathology and cognition will depend on the primary involvement of distinct parts of these circuits and on secondarily derived time-dependent disturbances of transmitter function. This review is focused on clinical and preclinical evidence for the impact of interactions between glutamatergic, dopaminergic, serotonergic and noradrenergic brain systems on cognitive performance. The hypothetical consequences of transmitter dysfunction for progressive development of impairment in sensorimotor gating are illustrated. Finally, the broad receptor profile of second generation antipsychotics is analysed to explain the clinical improvement in neurocognition that may occur during treatment with such drugs.
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Much controversy has surrounded the issue of whether clinical trials of new antipsychotic medications for the treatment of schizophrenia ought to include a placebo control group. On 18 September 1997, the authors co-chaired a symposium at the University of Toronto devoted to elucidating the issues relevant to this debate. Speakers with expertise in the areas of schizophrenia research, clinical trials methodology, medical ethics and informed consent presented their perspectives. This paper aims to summarize the major scientific and ethical issues raised during the symposium.